Open access peer-reviewed chapter

The Role of miR-107 in Prostate Cancer: A Review and Experimental Evidence

Written By

Maria Elizbeth Alvarez-Sanchez, Oscar Rojas Espinosa, Julio César Torres-Romero, Ereth Ameyatzin Robles Chávez, Edgar Estrella-Parra, María Dolores Ponce Regalado, Raúl Aragón Franco, Jose Gadú Campos Saucedo, Cesar López-Camarillo, Minerva Camacho Nuez and Verónica Fernández Sánchez

Submitted: February 27th, 2021 Reviewed: May 6th, 2021 Published: May 26th, 2021

DOI: 10.5772/intechopen.98281

Chapter metrics overview

137 Chapter Downloads

View Full Metrics


Over the past two decades, several research groups have focused on the functioning of microRNAs (miRNAs), because many of them function as positive or negative endogenous regulators of processes that alter during the development of cancer. Prostate cancer is the second most commonly occurring cancer in men. New biomarkers are needed to support the diagnosis of prostate cancer. Although it is necessary to deepen the research on this molecule to explore its potential utility in the diagnosis, follow-up, and prognosis of cancer, our results support a role of miR-107 in the signaling cascades that allow cancer progression, and as shown here, in the progression of Prostate Cancer (PCa). These findings strongly suggest that miR-107 may be a potential circulating biomarker for the diagnosis and prognosis of prostate cancer.


  • microRNAs
  • miR-107
  • biomarker
  • cancer hallmarks
  • therapeutic target

1. Introduction

Cancer can be defined as a state of uncontrolled cell-growth and dissemination that alters several cellular processes and functions [1]. Hanahan and Weinburg described, in 2000, six characteristics of cancer called “cancer hallmarks” that increased to ten in 2011 due to the complexity of the disease and the number of biological mechanisms that become altered. These cancer hallmarks include sustained proliferative signals, evading growth suppressors, avoidance of immune destruction, replicative immortality, tumor-promoting inflammation, sustained invasion and metastasis, induction of angiogenesis, genetic instability and mutation, resistance to cell death, and cell-metabolism deregulation [2].

Currently, more than 100 different types of cancer have been identified. According to the International Agency for Research in Cancer (IARC) in 2020, the most common types of cancer were those of lung, breast, prostate, colon, and stomach [3]. In the 2014 World Cancer Report, the World Health Organization (WHO) reported 14 million new cases and 8.2 million deaths in the year 2012 [4]. Last year, the Pan American Health Organization (PAHO) reported that in the Americas, the most frequently diagnosed types of cancer in men are prostate (21.7%), lung (9.5%), and colorectal (8.0%) cancer [5].

In 2018, the estimated number of new cases increased to 18 million, and it was expected that by 2030, more than 20 million cases will be registered annually [4]. Under this scenario, different methods of early diagnosis and treatment have been sought, which can effectively defeat the disease, leading to a significant reduction in the number of cases.


2. MicroRNAs as a potencial cancer biomarkers

MicroRNAs (miRNAs) are endogenous regulators of different biological processes, including those that are altered in cancer development such as cell growth and proliferation, differentiation, apoptosis, angiogenesis, and others [6]. miRNAs are a family of small non-coding RNAs, 18 to 22 nucleotides long whose function is the post-transcriptional regulation of gene expression [7]. They have a specific region composed of around 6 nucleotides called the seed region that binds the 3’UTR region of the target messenger RNA (mRNA). This union alters the stability of the transcript leading to its degradation or storage in intracellular structures called p-bodies, thus leading to effective repression of translation [8].

Different authors have reported that miRNAs have a tissue-specific expression pattern and that this pattern is altered in cancer tissues [9, 10]. Therefore, it has been suggested that these changes in the expression of miRNAs can be used as possible biomarkers of the disease [11]. However, the standard determination of the relative expression of miRNA requires a tissue sample from the cancer patient, which is considered a highly invasive process [12, 13]. Consequently, other diagnostic methods are required that are safe, effective, and accessible.

In 2008, Mitchell et al. described a specific type of miRNAs that were present in their stable form in different biological fluids, which they called circulating miRNAs (c-miRNAs) [14]. In their research, they analyzed the expression of different miRNAs in plasma, serum, and epithelial tissue samples. They observed that the miRNAs remained stable in serum and plasma, and in the tissue samples. They concluded that blood was a reliable source for the extraction and quantification of miRNAs. These findings have allowed the analysis of the expression of circulating miRNAs as a possible method for cancer diagnosis [14, 15].

There are more than 1000 miRNAs registered in the miRNA database (miRDB) that have been found in the human body; one of them is miR-107, which, according to miRDB, can have more than 800 possible targets [16].


3. Is miR-107, a circulating miRNA?

MicroRNA-107 (miR-107) is a molecule composed of 23 nucleotides; it is considered a c-miRNA because it can be found in a stable form in plasma and urine [17]. This miRNA is highly conserved in humans and other species. In humans, it is transcribed from the introns of the pantothenate kinase 1 gene, located on the long arm of chromosome 10 [16]. It belongs to the miR-103/107 family, which participates in the regulation of proteins involved in cell proliferation, cell cycle arrest, and programmed cell death or apoptosis [18].

Different research groups have reported that miR-107 is altered in different types of cancer in both men and women, including cervical [19], breast [20], ovary [21], colorectal [22], gastric [23], oral [24], penile [25], and prostate [13] cancers. Because of this, it has been proposed as a possible biomarker of cancer and a potential target for treatment.

So far, information on the expression of miR-107 in plasma has been published only on gastrointestinal cancer by Parvaee et al. [15], and in the urine of patients with prostate cancer by Lekchnov et al. [17]. Therefore, there is a great ​opportunity in this field to contribute to the design of new diagnostic methods for the detection of cancer from the early stages of the disease.


4. miR-107 and its participation in prostate cancer

PCa is the second leading cause of death in men over 45 years of age; the American Cancer Society estimates that 1 in 41 men will die this year from this cause. Nevertheless, prostate cancer has not been studied to the same extent as breast cancer, and hence, there is a lack of information on the development, evolution, and the treatment of this disease. Although the evaluation of prostatic specific antigen (PSA) has contributed to the early detection of PCa, its use may also lead to non-conclusive results because of false positive and negative results. Also, its low specificity can lead to misdiagnosis and incorrect treatment of indolent PCa patients [25, 26]. Patients with prostate cancer who receive radical treatment for presumably locally confined cancer can experience clinical relapses, indicating that the extent of these cancers was greater than the one previously diagnosed [27]. The median survival of metastatic PCa patients is 5 to 8 months, and their 5-year survival rate is less than 30%. This poor prognosis is the result of many factors including the lack of initial symptoms when PCa develops, local invasiveness, or metastases to distant organs in the early stage of the disease, and misdiagnosis [28, 29].

A majority of PCa patients who initially respond to androgen suppression treatment (AST) develop metastatic castration-resistant prostate cancer (CRPCa) within 2 years of treatment [29]. This condition still cannot be predicted, although several biomarkers have been tested (proteomic and metabolomic approaches) [30, 31]. This is mainly due to the wide variability of proteins being tested, the masking effect of abundant serum proteins, the high salt concentration in the samples, and the variability between individuals that drastically reduce the reproducibility of the biomarker’s determinations. miRNAs have been found to participate in the alteration of many cellular processes that lead to the development of cancer including proliferation [32, 33], differentiation [34, 35], angiogenesis, and evasion of apoptosis [36]. miRNAs can serve as biomarkers because they are resistant to degradation by RNases either in tumors or serum. miRNAs are small (18-24 nt), endogenous, non-coding RNAs, encoded either on intergenic regions of DNA or on introns and exons of genes that act as post-transcriptional control genes, triggering degradation or blocking translation of mRNAs by complementary base pairing [37]. When discovered, miRNAs were shown to control fundamental cellular processes, such as cell differentiation and timing of the organism development [38, 39], suggesting that aberrations of miRNAs could be involved in various human diseases, including cancer.

In recent years, several detailed studies have described the mechanisms through which miRNAs are stabilized and how they are detected in plasma and serum [10, 14]. Plasma/serum miRNAs are resistant to endogenous ribonuclease activity by binding to specific plasma proteins or by packing into various serum secretory vesicles, including apoptotic bodies and exosomes [14, 40, 41, 42]. Various blood-based miRNAs have been identified, including those in this study, and can be used for cancer detection, monitoring tumor dynamics, and predicting prognosis and chemoresistance [43, 44, 45, 46, 47].

Several reports have shown that changes in the level of circulating miRNAs associate with prostate cancer [48]. One of these miRNAs is miR-107, which is overexpressed by more than 11-fold in PCa [48] but whose role has not been studied in the context of cancer progression [49].

In 2019, Zhang et al. studied the role of miR-107 in prostate cancer in both the tissue and cancer cells (DU145 and PC3); they found that its levels decreased compared to the levels in healthy cells and tissue. Then they induced the overexpression of miR-107 and performed functional tests to evaluate its effects. In the colony formation test, they found that the increase in the expression of miR-107 significantly inhibited cell proliferation. They complemented this finding with the flow cytometric cell cycle test and concluded that the inhibition resulted from an arrest in the G1/S phase of the cycle, due to the binding of miR-107 to cyclin E1. In the migration and invasion tests, they did not find any influence of miR-107 on these cellular processes [13].

Previous studies show the tumorigenicity of the miR-107 family [50, 51, 52, 53]; thus, the inhibition of the expression of miR-107 might be a target for the treatment. miR-107 may promote the progression of prostate cancer to CRPCa, the end-stage of a multifactorial and heterogeneous disease process [54, 55]. Significant progress in understanding the molecular basis of CRPCa has been achieved in recent years [56] but despite this, CRPCa remains a lethal disease [57].

Recently, Liang et al. [58] reported that miR-107 induces chemoresistance in colorectal cancer (CRC) through the CAB39-AMPK-mTOR pathway, promoting metastasis. In this context, miR-107 levels could potentially be determined at the time of diagnosis to identify patients with aggressive disease/micro metastases and/or to predict recurrence following primary treatment.

Studies of Bryant et al. [48] strongly suggest that the presence of miR-107 in plasma can be used as a biomarker for cancer detection, monitoring, and prognosis predictor in PCa patients. They reported 12 miRNAs differentially expressed in the plasma of PCa patients compared to controls. Among these 12 miRNAs, 11 were significantly correlated with metastases. The association of two miRNAs, miR-141 and miR-375 with metastatic PCa was confirmed in a separate cohort. Furthermore, an analysis of urine revealed that miR-107 and miR-574-3p were also notably associated with PCa risk [48].

The role of miR-107 in other hallmarks of prostate cancer is not yet known. However, it would be relevant for the medical and scientific community to determine the participation of this miRNA in the development, growth, and metastasis of this disease; this will encourage further research tending to mitigate this pathology. The pleiotropic functions of miR-107 in diverse types of cancer indicate that it targets a variety of genes involved in tumor proliferation, invasiveness, metastasis, angiogenesis, and response to chemotherapy. Because of their carcinogenic or cancer-suppressor effects, miR107 can be used as a potential diagnostic and prognostic biomarker, or as a target for therapeutic intervention [48].


5. miR-107 and its participation in other urologic cancers

Both men and women can develop urological cancers, such as urethral, bladder, and kidney cancers. Other urologic cancers are gender specific. Males, besides the prostate, can experience testicular and penile cancer. The role of miR-107 in some of these cancers has not been reported previously.

Investigation of bladder cancer-related miRNAs shows a specific downregulation of miR-107 in the in-situcarcinoma lesions in comparison to a normal bladder [49]. Several studies have shown that miR-107 sponge effects could be involved in processes that upregulate circular RNAs (circRNA) in bladder cancer-related pathways. For example, overexpression of the circRNAs of the transcription factor (TCF) 25 (circ-TCF25) and transferrin receptor (TFRC) (circ-TFRC) negatively correlated with miR-107 promotes progression of bladder cancer through the circ-TCF25-miR-103a-3p/miR-107-CDK6 and circ-TFRC-miR-107-TFRC pathways, respectively [59, 60].

So far, only one study mentioning a relationship between miR-107 and kidney cancer has been published. Song et al. found that cell proliferation and invasiveness of renal cell carcinoma, which is the most common type of kidney cancer in adults, can be suppressed by high expression of miR-107 through an apparent cell cycle arrest at the G2/M phase [61]. In contrast, it has been found that high expression of miR-107 is frequently associated with a bad prognosis in patients with penile cancer [25]. Overexpression of miR-107 in penile cancer tissues was also reported by Zhang et al. [62].


6. Strategy and methodology of study of miR-107

While several techniques and methodologies have been used for the study of miR-107, the most used techniques are qRT-PCR, proliferation assays, Western blotting, luciferase reporter, and immunofluorescent and immunohistochemical assays (Figure 1, Table 1). Yet, other authors have used less conventional methodologies. Thus, the optimized electrochemical sensor technic enabled the PCR-free quantification of miR-375 in CaP cells with acceptable specificity, confirming its potential applicability for point care (POC) purposes [72]. Detection at attomole levels of miRNA in samples is possible by electrocatalytic detection using gold-loaded nanoporous superparamagnetic iron oxide nanocubes, that has proved successful in the detection of miR-107 from cancer cell lines [82]. Other authors mentioned the use of chromatographic techniques such as Liquid chromatography-mass spectrometry (LC–MS) to extract and identify polyphenols from the plant Hibiscus sabdarifa, which reduced the expression of miR-107 in the liver [63] as well as of osthole (a coumarin compound) which is neuroprotective [66], and polysaccharides from Agrimonia pilosa, which promote cell proliferation enhanced by miR-107 [78, 83].

Figure 1.

Methodology most frequently used in the study of miR-107.

Pre-analysisTechniques/molecular toolsPost-analysisAuthors
Organism/ pre-treatmentMethodologyStatistical analysisConclusions
Mice (LDLr −/−): fed a high-fat (liver tissue).
Hibiscus sabdarifa: polyphenols.
chromatography column, LC-MS, RT-PCR, Western blot, GC-MS, liver histology
to measure the lipid droplet content.
ANOVA,U Mann–Whitney, t-Student's, Fisher's test P< 0.05Polyphenols reduced the expression of miR-107 in the liver[63]
Human glioma tissue.
U251 and MO59K
cell line.
BALB/C-nu athymic nude mice.
qRT-PCR, transfection (miR-107), proliferation assay (MTT), Anchorage-independent growth assay, Cell apoptosis (annexing), luciferase reporter, Lentiviral construct transduction, Western blot and immunofluorescence analysis, computer-aided algorithms from PicTar.Student’s t-tests, Spearman’s rank correlation.
P< 0.05.
upregulation of miR-107 suppressed glioma
cell growth
HepG2 cells and HEK 293.cell transfection (miR-107), western blot, RT-PCR, DNA constructs, luciferase assay, Triglyceride assay,student's t-test. P<0.05miR-107 induced lipid accumulation in hepatocytes.[65]
52 tumor of
Kidney cancer.
HKC cell line.
Male nude mice
RT-PCR, Western blot, plasmid construction, transfection/infection, luciferase reporter assay, flow cytometricWilcoxon rank sum test, ANOVA, Student t test.miR-107 inhibit cell proliferation in renal cell carcinoma.[61]
Primary cortical neurons, HEK293 and SHSY5Y cells.
Osthole (7-methoxy-8- isopentenoxy coumarin)
Viral vector transduction, activity of LDH, cellular apoptosis (TUNEL), Immunofluorescence, RT-PCR, transfection (miR-107), western blot.ANOVA, Bonferroni’s, P< 0.05.Osthole is neuroprotective via up-regulate miR-107 in AD.[66]
SGC-7901, MKN-45, KATO III, BGC-823, AGS, MKN-28 and MKN1 cells lines.
male nude mice: implanted miRNA-107 (tumor)
Transfection (miRNA-107), si-RNA, plasmid, RT-PCR, wound healing assay, luciferase activity, Western blot.ANOVA, dunnett's multiple. P< 0.05miR-107 acts as tumor inhibitor for gastric cancer[67]
primary preadipocyte (mice)Plasmid vector, transfection, cDNA synthesis, qPCR, luciferase reporter assays, caspase-3 activity, flow cytometry (apoptosis), TUNEL, western bloth, immunofluorescent.Student’s t-test. P< 0.05 and < 0.01.miR-107 induced apoptosis pathway.[68]
SGBS cells:qPCR, western blotting, Transfected SGBS cells (miR-107, [3H]palmitic acid).not reportedmiR-107 reduces adipogenesis[69]
HCC patients:
1.FFPE cohort (tissue)
2. serum cohort (serum)
Patient receiving before cisplatin, lipiodol, doxorubicin.
qPCR. Total RNAChi-square test, Mann-Whitney U.
miR-107 is biomarkers for predication of TACE treatment outcomes in HCC patients.[70]
42 OA patients (cartilage samples): chondrocytes
48 rats: establish OA
Transfection (chondrocytes/miR-107), flow cytometry, apoptosis (annexin/TUNEL assay), luciferase reporter, western blot, RT-q PCR,Student's t-test.
miR-107 induced apoptosis and autophagy of OA chondrocytes[71]
PC-3, DU145, LNCaP,
267B1, X/267B1, and Ki/267B1 cells
RNA isolation, qRT-PCR, electrochemical measurements (CHI 660D electrochemical workstation): frequency range of 0.1 Hz to 100 kHz with an alternating current amplitude of 10 mV.Student's t-test. P< 0.05Viability of the electrochemical evaluation method in clinical environment.[72]
75 ADHD patients: stimulation in rDLPFC. for 6 weeks:
18 healthy children.
Venous blood in both case.
RNA extraction, serum miRNA extraction, miRNA reverse transcription, fluorescence qPCR.Mann-Whitney U test or Student's t-test. P< 0.05serum miRNA-let-7d in ADHD
patients is higher as compared to healthy children.
SKOV3 and 293T cells; transfected with lentivirusesqRT-PCR, luciferase report assay, western blot, xenograft model and immunohistochemistry assay.ANOVA, Student's t test, P<0.05miR-107 as a tumor suppressor in ovarian cancer.[74]
Patients with AD.
SH-SY5Y and PC12 cells
Mouse model: introducing 6-OHDA into the right ventral tegmental area
Cell transfection, qPCR, caspase-3 activity (ELISA), ROS, LDH, SOD, luciferase reporter assay, western blot. Rota-rod test.
patients with AD: motor imagery test
Tukey's test,
P< 0.05.
miR-107 may be a therapeutic target for the treatment of AD-related impairments.[75]
HT-22 cell linecoimmunoprecipitation, chromatin immunoprecipitation, Luciferase reporter, qRT-PCR, apoptosis
detection (annexin), western blot.
t-test, ANOVA, Tukey's test
P< 0.05
RMST activates p53/miR-107 signaling pathway[76]
Serum samples (NSCLC).
cell line BESA-2B, NSCLC, A549, H1299, HCC827, PC-9, 95-D, H1975, HEK-293T
luciferase reporter gene, qRT-PCR, western blot, Immunohistochemistry.t-tests for two-group comparisonsP< 0.05.miR-107 could inhibit the progression of
40 Sprague Dawley (SD) rats.
MC3T3-E1 cells
Agrimonia pilos(isolated polysaccharide)
Rats induced SANFH (dex)
Femoral head tissue: apoptosis cellular (TUNEL), RT-PCR, cell proliferation (annexin), MC3T3-E1 cells transfected with anti-miR-107, flow cytometry, ALP activity, western blot.ANOVA. P< 0.05polysaccharides promote cell proliferation/ osteogenic differentiation by enhancing miR-107[78]
HeLa and HEKReporter gene assay (FuGENE 6), RT-PCR, immunoblot/ Immunofluorescence assay, chromatin immunoprecipitation,
ChIP-seq analysis: microRNA103–3p/107 target,. motif discovery (RSAT), Gene ontology analysis, genomic distribution (CEAS), siRNA transfections.
ANOVA, Bonferroni, KruskalWallis, Dunn’s, t-test, Mann-Whitney U. P< 0.05.miR-107 is potent regulators of GR function[79]
30 HIBD rats
Neonatal male Sprague-Dawley: HIBD
injected with adenovirus: primary neuron cells
Neuronal cells (infected with adenovirus): RT-qPCR, Protein extraction, western blot, luciferase reporter, immunofluorescence, fluorescent hybridization, RNA immunoprecipitation. hippocampal neurons (NisslStaining).unpaired t-test, ANOVA,
Tukey test.
P < 0.05.
miR-107 network has the potential to provide novel
insights into treatment targets for HIBD.
70 tumor human tissue (NPC)
Fresh frozen cell lines: HNE1, HONE1, 5–8F, 6–10B, and C666-1 and NP69:
qRT-PCR, western blot, cell apoptosis (anexin), flow cytometry, DIG-UTP-labeled miR-107, FISH kit, Immunofluorescence/ Immunohistochemical analysis
BALB/c mice: (transfected HNE1 cells) lung
Student’s t-test/Chi-square test, Pearson correlation. P< 0.05circTGFBR2 suppresses the proliferation,
migration, and invasiveness of NPC cells by sponging miR-

Table 1.

Methodology and techniques used in the study of miR-107.

HIBD: hypoxic-ischemic brain damage. NPC: nasopharyngeal carcinoma. NP69: immortalized nasopharyngeal epithelial cell line. RT-qPCR: quantitative polymerase chain reaction. HeLa: Human cervical carcinoma cells. HEK: human embryonic kidney cells. GR: glucocorticoids. SANFH: steroid-induced osteonecrosis of the femoral head. Dex: dexamethasone. ALP: Alkaline phosphatase. BESA-2B, NSCLC, A549, H1299, HCC827, PC-9, 95-D, H1975: Human normal bronchial epithelial cell line: HEK-293T: human embryonic kidney cell line. NSCLC: Non-small cell lung cancer. TGFβR2: Transforming growth factor β receptor 2. HT-22: Immortalized mouse hippocampal neuron cell line. RMST: rhabdomyosarcoma 2-associated transcript. hnRNPK: Heterogeneous nuclear ribonucleoprotein K. SH-SY5Y: human neuroblastoma cell line. PC12: cells rat pheochromocytoma. LDH lactate dehydrogenase release. SOD: superoxide dismutase. ROS: reactive oxygen species. 6-OHDA: 6-hydroxydopamine. fMRI: magnetic resonance imaging. AD: Alzheimer's disease. ADHD: attention deficit hyperactivity disorder. rDLPFC: right dorsolateral prefrontal cortex. A549: human lung carcinoma cells. Human_Br07: human-origin seasonal influenza A virus H3N2. PC-3, DU145 and LNCaP: human transformed prostate epithelial cell lines. 267B1, X/267B1: cell line nontumorigenic in nude mice. Ki/267B1: cell line moderately tumorigenic nontumorigenic in nude mice. OA: Osteoarthritis. TRAF3: TNF Receptor Associated Factor 3. HCC: hepatocellular carcinoma. FFPE: Formalin-Fixed Paraffin-Embedded. TACE: transcatheter arterial chemoembolization (cancerous tumor therapy). SGBS: Simpson-Golabi-Behmel syndrome preadipocytes. LDLr -/-: deficient in LDL receptor. LC-MS: Liquid chromatography–mass spectrometry. GC-MS: Gas chromatography–mass spectrometry. U251 and MO59K: Human glioma cell lines. MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide. SALL4: Sal-like 4. HKC: Human renal proximal tubular epithelial cell line. SHSY5Y: neuron cell line. SGC-7901, MKN-45, KATO III, BGC-823, AGS, MKN-28 and MKN1: gastric cancer cell lines. TGFBR2: transforming growth factor-β receptor II.

A variety of statistical tests have been used to validate the results, including parametric (ANOVA, student-t, Tukey) and non-parametric (Mann–Whitney U, Kruskal Wallis, Bonferroni, Dunn’s multiple comparison, Chi-square, and Pearson correlation) tests. The probability level in all cases have been P < 0.05. In conclusion, the new technology and the use of diverse statistical tools validate the study and significance of mirR-107 in diverse biological situations, including CaP.


7. miR-107 as a possible blood biomarker

In 2019, Parvaee et al., evaluated the expression of three miRNAs, including miR-107, in blood samples from 50 patients with gastrointestinal cancer. After extracting and analyzing the plasma, they observed that the expression of miR-107 was significantly lower in patients with this type of cancer, compared to healthy volunteers (93.8% sensitivity and 78.8% specificity). From the ROC curve evaluation, they found that the patients could be distinguished from healthy people at cutoff levels of 0.504 (miR-107), 0.266 (miR-194), and 0.394 (miR-210). Finally, they concluded that miR-107 could serve as a possible plasma biomarker, assuring the minimum degree of invasion for the patient and an adequate level of reliability in the diagnosis [15].


8. The future for the miR-107

Given its role in cell cycle arrest and its direct involvement in cancer, the therapeutic potential of miR-107 is anticipated [13]. miR-107 may be a key target for the treatment of prostate cancer, arresting tumor growth, and cell survival.


9. Conclusion

The findings condensed in this review enable us to envisage miR-107 as a biomarker and possible therapeutic target for diverse types of prostate cancer. Although it is necessary to deepen the research on this molecule to explore its potential utility in the diagnosis, follow-up, and prognosis of cancer, our results support a role of miR-107 in the signaling cascades that allow cancer progression, and as shown here, in the progression of PCa to CRPCa. Our research suggests a potential utility of miR-107 as an accurate tool for diagnoses and follow-up of PCa.



We acknowledge the Universidad Autónoma de la Ciudad de México (UACM), the Colegio de Ciencia y Tecnología of the UACM (project number PI-CCyT-2019-07), and the Secretaría de Posgrado e Investigación (SEPI) de la Escuela Nacional de Ciencias Biológicas del Instituto Politécnico Nacional, for their support in producing this article.

Conflict of interest

The authors declare that they have no competing interests.

Funding information

The present study was funded by Universidad Autónoma de la Ciudad de México and the Consejo Nacional de Ciencia y Tecnología (CONACYT) (scholarship 734919 to EARC), and the Colegio de Ciencia y Tecnología of the UACM project PI-CCyT-2019-07 (19-09-4000.001-000-000-000-7100-0010).

Author’s contribution

MEAS, EARC, and EEP conceived, designed, and wrote the review. ORE, CLC, MDPR, JCTR, MCN and RAF reviewed and edited the manuscript. All authors read and approved the manuscript and agreed to be accountable for all aspects of the research ensuring that the accuracy or integrity of any part of the work is appropriately investigated and resolved.


  1. 1. Hanahan D, Weinberg RA. The hallmarks of cancer.Cell. Published online 2000. doi:10.1016/S0092-8674(00)81683-9
  2. 2. Hanahan D, Weinberg RA. Hallmarks of cancer: The next generation.Cell. Published online 2011. doi:10.1016/j.cell.2011.02.013
  3. 3. The most common types of cancer [Internet]. 2021. Available from:[Accessed: 2021-03-01]
  4. 4. World Cancer Report 2014 [Internet]. 2020. Available from:[Accessed: 2020-07-01]
  5. 5. World Cancer Day: I Am and I Will [Internet]. 2021. Available from:[Accessed: 2021-03-01]
  6. 6. Liu F, Liu S, Ai F, et al. MiR-107 promotes proliferation and inhibits apoptosis of colon cancer cells by targeting prostate apoptosis response-4 (Par4). Oncol Res. 2017;25(6):967-974. doi:10.3727/096504016X14803476672380
  7. 7. Bartel DP. MicroRNAs: Genomics, Biogenesis, Mechanism, and Function.Cell. Published online 2004. doi:10.1016/S0092-8674(04)00045-5
  8. 8. Lin S, Gregory RI. MicroRNA biogenesis pathways in cancer. Nat Rev Cancer. 2015;15(6):321-333. doi:10.1038/nrc3932
  9. 9. Lu J, Getz G, Miska EA, et al. MicroRNA expression profiles classify human cancers. Nature. 2005;435(7043):834-838. doi:10.1038/nature03702
  10. 10. Calin GA, Croce CM. MicroRNA signatures in human cancers.Nat Rev Cancer. Published online 2006. doi:10.1038/nrc1997
  11. 11. Sita-Lumsden A, Dart DA, Waxman J, Bevan CL. Circulating microRNAs as potential new biomarkers for prostate cancer.Br J Cancer. Published online 2013. doi:10.1038/bjc.2013.192
  12. 12. Norma Oficial Mexicana NOM-025-SSA3-2013, Para la organización y funcionamiento de las unidades de cuidados intensivos - 17 de Septiembre de 2013 - DOF. Diario Oficial de la Federación - Legislación - VLEX 461013722. Accessed December 2, 2020.
  13. 13. Zhang X, Jin K, Luo JD, Liu B, Xie LP. MicroRNA-107 inhibits proliferation of prostate cancer cells by targeting cyclin E1. Neoplasma. 2019;66(5):704-716. doi:10.4149/neo_2018_181105N825
  14. 14. Mitchell PS, Parkin RK, Kroh EM, et al. Circulating microRNAs as stable blood-based markers for cancer detection.Proc Natl Acad Sci U S A. Published online 2008. doi:10.1073/pnas.0804549105
  15. 15. Parvaee P, Sarmadian H, Khansarinejad B, Amini M, Mondanizadeh M. Plasma level of microRNAs, miR-107, miR-194 and miR-210 as potential biomarkers for diagnosis intestinal-type gastric cancer in human.Asian Pacific J Cancer Prev. 2019;20(5):1421-1426. doi:10.31557/APJCP.2019.20.5.1421
  16. 16. hsa-miR-107 targets [Internet]. 2020. Available from:[Accessed: 2020-07-01]
  17. 17. Lekchnov EA, Amelina E V., Bryzgunova OE, et al. Searching for the novel specific predictors of prostate cancer in urine: The analysis of 84 miRNA expression.Int J Mol Sci. Published online 2018. doi:10.3390/ijms19124088
  18. 18. Yu QF, Liu P, Li ZY, et al. MiR-103/107 induces tumorigenicity in bladder cancer cell by suppressing PTEN.Eur Rev Med Pharmacol Sci. 2018;22(24):8616-8623. doi:10.26355/eurrev_201812_16625
  19. 19. Zhou C, Li G, Zhou J, Han N, Liu Z, Yin J. Mir-107 activates ATR/chk1 pathway and suppress cervical cancer invasion by targeting MCL. PLoS One. 2014;9(11):111860. doi:10.1371/journal.pone.0111860
  20. 20. Ai H, Zhou W, Wang Z, Qiong G, Chen Z, Deng S. microRNAs-107 inhibited autophagy, proliferation, and migration of breast cancer cells by targeting HMGB1. J Cell Biochem. 2019;120(5):8696-8705. doi:10.1002/jcb.28157
  21. 21. Tang Z, Fang Y, Du R. MicroRNA-107 induces cell cycle arrests by directly targeting cyclin E1 in ovarian cancer. Biochem Biophys Res Commun. 2019;512(2):331-337. doi:10.1016/j.bbrc.2019.03.009
  22. 22. Fu Y, Lin L, Xia L. MiR-107 function as a tumor suppressor gene in colorectal cancer by targeting transferrin receptor 1.Cell Mol Biol Lett. 2019;24(1). doi:10.1186/s11658-019-0155-z
  23. 23. Wang L, Li K, Wang C, Shi X, Yang H. miR-107 regulates growth and metastasis of gastric cancer cells via activation of the PI3K-AKT signaling pathway by down-regulating FAT4. Cancer Med. 2019;8(11):5264-5273. doi:10.1002/cam4.2396
  24. 24. Na C, Li X, Zhang J, Han L, Li Y, Zhang H.MiR-107 Targets TRIAP1 to Regulate Oral Squamous Cell Carcinoma Proliferation and Migration. Vol 12. e-Century Publishing Corporation; 2019
  25. 25. Pinho JD, Silva GEB, Teixeira Júnior AAL, et al. MIR-107, MIR-223-3P and MIR-21-5P Reveals Potential Biomarkers in Penile Cancer.Asian Pac J Cancer Prev. 2020;21(2):391-397. doi:10.31557/APJCP.2020.21.2.391
  26. 26. Ciatto S, Zappa M, Bonardi R, Gervasi G. Prostate cancer screening: The problem of overdiagnosis and lessons to be learned from breast cancer screening.Eur J Cancer. Published online 2000. doi:10.1016/S0959-8049(00)00119-2
  27. 27. Dall’era MA, Cooperberg MR, Chan JM, et al. Active surveillance for early-stage prostate cancer: Review of the current literature.Cancer. Published online 2008. doi:10.1002/cncr.23373
  28. 28. Heinemann V, Boeck S, Hinke A, Labianca R, Louvet C. Meta-analysis of randomized trials: Evaluation of benefit from gemcitabine-based combination chemotherapy applied in advanced pancreatic cancer.BMC Cancer. Published online 2008. doi:10.1186/1471-2407-8-82
  29. 29. Jemal A, Siegel R, Ward E, Hao Y, Xu J, Thun MJ. Cancer Statistics, 2009.CA Cancer J Clin. Published online 2009. doi:10.3322/caac.20006
  30. 30. Sultana A, Tudur Smith C, Cunningham D, Starling N, Neoptolemos JP, Ghaneh P. Meta-analyses of chemotherapy for locally advanced and metastatic pancreatic cancer: Results of secondary end points analyses.Br J Cancer. Published online 2008. doi:10.1038/sj.bjc.6604436
  31. 31. Loriot Y, Massard C, Fizazi K. Recent developments in treatments targeting castration-resistant prostate cancer bone metastases.Ann Oncol. Published online 2012. doi:10.1093/annonc/mdr573
  32. 32. Velonas VM, Woo HH, dos Remedios CG, Assinder SJ. Current status of biomarkers for prostate cancer.Int J Mol Sci. Published online 2013. doi:10.3390/ijms140611034
  33. 33. Karrich JJ, Jachimowski LCM, Libouban M, et al. MicroRNA-146a regulates survival and maturation of human plasmacytoid dendritic cells.Blood. Published online 2013. doi:10.1182/blood-2012-12-475087
  34. 34. Xu XH, Li DW, Feng H, Chen HM, Song YQ. MiR-300 regulate the malignancy of breast cancer by targeting p53.Int J Clin Exp Med. Published online 2015
  35. 35. Maebayashi T, Abe K, Aizawa T, et al. Solitary pulmonary metastasis from prostate cancer with neuroendocrine differentiation: A case report and review of relevant cases from the literature.World J Surg Oncol. Published online 2015. doi:10.1186/s12957-015-0598-2
  36. 36. Baltimore D, Boldin MP, O’Connell RM, Rao DS, Taganov KD. MicroRNAs: New regulators of immune cell development and function.Nat Immunol. Published online 2008. doi:10.1038/ni.f.209
  37. 37. Jerónimo C, Bastian PJ, Bjartell A, et al. Epigenetics in prostate cancer: Biologic and clinical relevance.Eur Urol. Published online 2011. doi:10.1016/j.eururo.2011.06.035
  38. 38. Brase JC, Johannes M, Schlomm T, et al. Circulating miRNAs are correlated with tumor progression in prostate cancer.Int J Cancer. Published online 2011. doi:10.1002/ijc.25376
  39. 39. He L, Hannon GJ. MicroRNAs: Small RNAs with a big role in gene regulation.Nat Rev Genet. Published online 2004. doi:10.1038/nrg1379
  40. 40. Kosaka N, Iguchi H, Ochiya T. Circulating microRNA in body fluid: A new potential biomarker for cancer diagnosis and prognosis.Cancer Sci. Published online 2010. doi:10.1111/j.1349-7006.2010.01650.x
  41. 41. Hasselmann DO, Rappl G, Tilgen W, Reinhold U. Extracellular tyrosinase mRNA within apoptotic bodies is protected from degradation in human serum.Clin Chem. Published online 2001. doi:10.1093/clinchem/47.8.1488
  42. 42. Cocucci E, Racchetti G, Meldolesi J. Shedding microvesicles: Artefacts no more. Trends Cell Biol. 2009;19(2):43-51. doi:10.1016/j.tcb.2008.11.003
  43. 43. Tsujiura M, Komatsu S, Ichikawa D, et al. Circulating miR-18a in plasma contributes to cancer detection and monitoring in patients with gastric cancer. Gastric Cancer. 2015;18(2):271-279. doi:10.1007/s10120-014-0363-1
  44. 44. Kawaguchi T, Komatsu S, Ichikawa D, et al. Circulating microRNAS: A next-generation clinical biomarker for digestive system cancers.Int J Mol Sci. Published online 2016. doi:10.3390/ijms17091459
  45. 45. Komatsu S, Ichikawa D, Kawaguchi T, et al. Plasma microRNA profiles: Identification of miR-23a as a novel biomarker for chemoresistance in esophageal squamous cell carcinoma.Oncotarget. Published online 2016. doi:10.18632/oncotarget.11500
  46. 46. Reinhart BJ, Slack FJ, Basson M, et al. The 21-nucleotide let-7 RNA regulates developmental timing inCaenorhabditis elegans.Nature. Published online 2000. doi:10.1038/35002607
  47. 47. Michael MZ, O’Connor SM, Van Holst Pellekaan NG, Young GP, James RJ. Reduced Accumulation of Specific MicroRNAs in Colorectal Neoplasia.Mol Cancer Res. Published online 2003
  48. 48. Bryant RJ, Pawlowski T, Catto JWF, et al. Changes in circulating microRNA levels associated with prostate cancer.Br J Cancer. Published online 2012. doi:10.1038/bjc.2011.595
  49. 49. Catto JWF, Miah S, Owen HC, et al. Distinct MicroRNA alterations characterize high- and low-grade bladder cancer.Cancer Res. Published online 2009. doi:10.1158/0008-5472.CAN-09-0744
  50. 50. Chen H-Y, Lin Y-M, Chung H-C, et al. miR-103/107 Promote Metastasis of Colorectal Cancer by Targeting the Metastasis Suppressors DAPK and KLF4.Cancer Res. 2012;72(14):3631 LP - 3641. doi:10.1158/0008-5472.CAN-12-0667
  51. 51. Zheng J, Liu Y, Qiao Y, Zhang L, Lu S. miR-103 Promotes Proliferation and Metastasis by Targeting KLF4 in Gastric Cancer.Int J Mol Sci. 2017;18(5):910. doi:10.3390/ijms18050910
  52. 52. Xiong B, Lei X, Zhang L, Fu J. miR-103 regulates triple negative breast cancer cells migration and invasion through targeting olfactomedin 4.Biomed Pharmacother. 2017;89:1401-1408. doi:
  53. 53. Xiong J, Wang D, Wei A, et al. Deregulated expression of miR-107 inhibits metastasis of PDAC through inhibition PI3K/Akt signaling via caveolin-1 and PTEN. Exp Cell Res. 2017;361(2):316-323. doi:
  54. 54. deVere White RW, Vinall RL, Tepper CG, Shi X-B. MicroRNAs and their potential for translation in prostate cancer. Urol Oncol Semin Orig Investig. 2009;27(3):307-311. doi:
  55. 55. Shi X-B, Xue L, Yang J, et al. An androgen-regulated miRNA suppresses Bak1 expression and induces androgen-independent growth of prostate cancer cells.Proc Natl Acad Sci. 2007;104(50):19983 LP - 19988. doi:10.1073/pnas.0706641104
  56. 56. Lin SL, Chiang A, Chang D, Ying SY. Loss of mir-146a function in hormone-refractory prostate cancer.RNA. Published online 2008. doi:10.1261/rna.874808
  57. 57. Sun T, Wang Q , Balk S, Brown M, Lee GSM, Kantoff P. The role of microrna-221 and microrna-222 in Androgen- independent prostate cancer cell lines.Cancer Res. Published online 2009. doi:10.1158/0008-5472.CAN-08-4112
  58. 58. Liang Y, Zhu D, Hou L, et al. MiR-107 confers chemoresistance to colorectal cancer by targeting calcium-binding protein 39.Br J Cancer. Published online 2020. doi:10.1038/s41416-019-0703-3
  59. 59. Zhong Z, Lv M, Chen J. Screening differential circular RNA expression profiles reveals the regulatory role of circTCF25-miR-103a-3p/miR-107-CDK6 pathway in bladder carcinoma. Sci Rep. 2016;6. doi:10.1038/srep30919
  60. 60. Su H, Tao T, Yang Z, et al. Circular RNA cTFRC acts as the sponge of MicroRNA-107 to promote bladder carcinoma progression. Mol Cancer. 2019;18(1):27. doi:10.1186/s12943-019-0951-0
  61. 61. Song N, Ma X, Li H, et al. MicroRNA-107 functions as a candidate tumor suppressor gene in renal clear cell carcinoma involving multiple genes.Urol Oncol Semin Orig Investig. Published online 2015. doi:10.1016/j.urolonc.2015.02.003
  62. 62. Zhang L, Wei P, Shen X, et al. MicroRNA expression profile in penile cancer revealed by next-generation small RNA sequencing.PLoS One. Published online 2015. doi:10.1371/journal.pone.0131336
  63. 63. Joven J, Espinel E, Rull A, et al. Plant-derived polyphenols regulate expression of miRNA paralogs miR-103/107 and miR-122 and prevent diet-induced fatty liver disease in hyperlipidemic mice. Biochim Biophys Acta - Gen Subj. 2012;1820(7):894-899. doi:10.1016/j.bbagen.2012.03.020
  64. 64. He J, Zhang W, Zhou Q , et al. Low-expression of microRNA-107 inhibits cell apoptosis in glioma by upregulation of SALL4.Int J Biochem Cell Biol. Published online 2013. doi:10.1016/j.biocel.2013.06.008
  65. 65. Bhatia H, Verma G, Datta M. MiR-107 orchestrates ER stress induction and lipid accumulation by post-transcriptional regulation of fatty acid synthase in hepatocytes.Biochim Biophys Acta - Gene Regul Mech. Published online 2014. doi:10.1016/j.bbagrm.2014.02.009
  66. 66. Jiao Y, Kong L, Yao Y, et al. Osthole decreases beta amyloid levels through up-regulation of miR-107 in Alzheimer’s disease.Neuropharmacology. Published online 2016. doi:10.1016/j.neuropharm.2016.04.046
  67. 67. Cheng F, Yang Z, Huang F, Yin L, Yan G, Gong G. microRNA-107 inhibits gastric cancer cell proliferation and metastasis by targeting PI3K/AKT pathway. Microb Pathog. 2018;121:110-114. doi:10.1016/j.micpath.2018.04.060
  68. 68. Zhang Z, Wu S, Muhammad S, Ren Q , Sun C. miR-103/107 promote ER stress-mediated apoptosis via targeting the Wnt3a/−catenin/ATF6 pathway in preadipocytes. J Lipid Res. 2018;59(5):843-853. doi:10.1194/jlr.M082602
  69. 69. Ahonen MA, Haridas PAN, Mysore R, Wabitsch M, Fischer-Posovszky P, Olkkonen VM. miR-107 inhibits CDK6 expression, differentiation, and lipid storage in human adipocytes.Mol Cell Endocrinol. Published online 2019. doi:10.1016/j.mce.2018.09.007
  70. 70. Ali HEA, Emam AA, Zeeneldin AA, et al. Circulating miR-26a, miR-106b, miR-107 and miR-133b stratify hepatocellular carcinoma patients according to their response to transarterial chemoembolization.Clin Biochem. Published online 2019. doi:10.1016/j.clinbiochem.2019.01.002
  71. 71. Zhao X, Li H, Wang L. MicroRNA-107 regulates autophagy and apoptosis of osteoarthritis chondrocytes by targeting TRAF3.Int Immunopharmacol. Published online 2019. doi:10.1016/j.intimp.2019.03.005
  72. 72. Jeong B, Kim YJ, Jeong JY, Kim YJ. Label-free electrochemical quantification of microRNA-375 in prostate cancer cells.J Electroanal Chem. Published online 2019. doi:10.1016/j.jelechem.2019.05.009
  73. 73. Cao P, Wang L, Cheng Q , et al. Changes in serum miRNA-let-7 level in children with attention deficit hyperactivity disorder treated by repetitive transcranial magnetic stimulation or atomoxetine: An exploratory trial.Psychiatry Res. Published online 2019. doi:10.1016/j.psychres.2019.02.037
  74. 74. Tang Z, Fang Y, Du R. MicroRNA-107 induces cell cycle arrests by directly targeting cyclin E1 in ovarian cancer.Biochem Biophys Res Commun. Published online 2019. doi:10.1016/j.bbrc.2019.03.009
  75. 75. Sun L, Zhang T, Xiu W, et al. MiR-107 overexpression attenuates neurotoxicity induced by 6-hydroxydopamine both in vitro and in vivo.Chem Biol Interact. Published online 2020. doi:10.1016/j.cbi.2019.108908
  76. 76. Cheng H, Sun M, Wang ZL, et al. LncRNA RMST-mediated miR-107 transcription promotes OGD-induced neuronal apoptosis via interacting with hnRNPK.Neurochem Int. Published online 2020. doi:10.1016/j.neuint.2019.104644
  77. 77. Wu Z, Yuan Q , Yang C, et al. Downregulation of oncogenic gene TGFβR2 by miRNA-107 suppresses non-small cell lung cancer.Pathol Res Pract. 2020;216(1). doi:10.1016/j.prp.2019.152690
  78. 78. Huang W, Jin S, Yang W, et al. Agrimonia pilosa polysaccharide and its sulfate derives facilitate cell proliferation and osteogenic differentiation of MC3T3-E1 cells by targeting miR-107.Int J Biol Macromol. Published online 2020. doi:10.1016/j.ijbiomac.2019.11.213
  79. 79. Yang N, Berry A, Sauer C, et al. Hypoxia regulates GR function through multiple mechanisms involving microRNAs 103 and 107.Mol Cell Endocrinol. Published online 2020. doi:10.1016/j.mce.2020.111007
  80. 80. Fang H, Li H-F, Pan Q , et al. Long noncoding RNA H19 overexpression protects against hypoxic-ischemic brain damage by inhibiting miR-107 and up-regulating vascular endothelial growth factor. Am J Pathol. 2021;191(3):503-514. doi:10.1016/j.ajpath.2020.11.014
  81. 81. Li W, Lu H, Wang H, et al. Circular RNA TGFBR2 acts as a ceRNA to suppress nasopharyngeal carcinoma progression by sponging miR-107.Cancer Lett. Published online 2021. doi:10.1016/j.canlet.2020.11.001
  82. 82. Islam MN, Masud MK, Nguyen NT, et al. Gold-loaded nanoporous ferric oxide nanocubes for electrocatalytic detection of microRNA at attomolar level.Biosens Bioelectron. Published online 2018. doi:10.1016/j.bios.2017.09.027
  83. 83. Huang W, Deng H, Jin S, Ma X, Zha K, Xie M. The isolation, structural characterization and anti-osteosarcoma activity of a water soluble polysaccharide from Agrimonia pilosa.Carbohydr Polym. Published online 2018. doi:10.1016/j.carbpol.2018.01.047

Written By

Maria Elizbeth Alvarez-Sanchez, Oscar Rojas Espinosa, Julio César Torres-Romero, Ereth Ameyatzin Robles Chávez, Edgar Estrella-Parra, María Dolores Ponce Regalado, Raúl Aragón Franco, Jose Gadú Campos Saucedo, Cesar López-Camarillo, Minerva Camacho Nuez and Verónica Fernández Sánchez

Submitted: February 27th, 2021 Reviewed: May 6th, 2021 Published: May 26th, 2021