• Users Online: 6865
  • Print this page
  • Email this page

Table of Contents
Year : 2019  |  Volume : 6  |  Issue : 1  |  Page : 1-6

The roles of microRNA-331 Family in Cancers

1 Department of Human Biology, International Medical University, Kuala Lumpur, Malaysia
2 Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Selangor, Malaysia

Date of Submission10-Jun-2018
Date of Decision25-Sep-2018
Date of Acceptance27-Sep-2018
Date of Web Publication1-Mar-2019

Correspondence Address:
Dr. Khuen Yen Ng
Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Jalan Lagoon Selatan, Bandar Sunway, 47500 Subang Jaya, Selangor
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JCRP.JCRP_6_18

Rights and Permissions

MicroRNAs (miRNAs) are single-stranded noncoding RNA strands that are involved in various pathological and physiological processes. Even though they do not code for any gene, they regulate gene expression by posttranscriptional modification through cleavage or translational repression of messenger RNA. Many miRNAs (for example, lethal-7 and miRNA-21) have been found to be involved in the pathogeneses of many diseases including cancers. The miRNA-331 family includes three miRNAs, namely, miRNA-331, miRNA-331-3p, and miRNA-331-5p. Recent studies have revealed that the miRNA-331 family is associated with the pathology of some cancers, including colorectal cancer, leukemia, hepatocellular carcinoma, prostate cancer, pancreatic cancer, breast cancer, melanoma, and lung cancer. Therefore, it is important to have a good understanding about how the miRNA-331 family regulates the pathogeneses of these cancers. In this review, we discuss the pathological and physiological roles of the miRNA-331 family. Understanding how these miRNAs regulate the gene expression levels of their targets and their involvement in cancers may lead to better therapeutic strategies to treat cancers.

Keywords: Cancer, microRNA, noncoding RNA

How to cite this article:
Shee SM, Koh RY, Voon KG, Chye SM, Othman I, Ng KY. The roles of microRNA-331 Family in Cancers. J Cancer Res Pract 2019;6:1-6

How to cite this URL:
Shee SM, Koh RY, Voon KG, Chye SM, Othman I, Ng KY. The roles of microRNA-331 Family in Cancers. J Cancer Res Pract [serial online] 2019 [cited 2022 Dec 5];6:1-6. Available from: https://www.ejcrp.org/text.asp?2019/6/1/1/253249

  Introduction Top

Since the discovery of DNA in 1958 by Francis Crick, it has been known that human genetic information is present in DNA, and that it is responsible for the transcription process to form messenger RNA (mRNA). mRNA acts as the blueprint for the formation of specific amino acid sequences, leading to the production of specific proteins.[1] In the 1960s, noncoding RNAs (ncRNAs) with a close resemblance to mRNA in length and splicing patterns were also discovered. They were found to house classes of RNA transcripts that act as RNA molecules instead of coding for any proteins.[2] Further, it was found that ncRNAs also regulate the transcription and translation processes of protein-coding genes.[1],[3],[4] Other than small ncRNAs, large ncRNAs have also been discovered in the human genome. An example of a functional large ncRNA is the X-inactive-specific transcript, that is exclusively expressed from an inactive X chromosome and works as a silencing agent for the entire X chromosome in females.[1],[5]

Evidence has shown that ncRNAs participate in both physiological and pathological processes. In a normal person, 75% of the human genome is transcribed into RNA with only 3% being transcribed into mRNAs with protein-coding elements present within. Hence, ncRNAs are far more abundant than the RNAs of the normal-protein coding genes.[6] Considering the regulatory role and high abundance of ncRNAs in the human body, they are considered to be potential biomarkers or therapeutic targets for various diseases.[7],[8],[9],[10],[11] Several types of ncRNAs have been identified, including microRNAs (miRNAs), small interfering RNAs (siRNAs), and Piwi-associated RNAs.[1],[12] Among these, the roles of miRNAs have been frequently investigated since the discovery of their involvement in cancer development.[4] In addition, other studies have indicated their involvement in embryonic development and regulation of the immune system.[13],[14] miRNAs have gained much attention and recognition due to their roles in epigenetic processes, cellular communication, human physiology, pathology of diseases, and therapies.[1],[4],[14],[15]

miRNA was first identified from the lin-4 gene of the parasite Caenorhabditis.[1],[15] It was noticed in Caenorhabditis elegans that the lin-4 gene produces an antisense oligonucleotide complementary to multiple sites present in the 3'-untranslated region (UTR) of the lin-14 gene; and that through this antisense mechanism lin-14 was repressed by lin-4. These findings triggered further interest in the roles of these complementary sites in the regulation of lin-14 by lin-4.[3] Later, it was found that lin-4 only regulates lin-14 at the protein translation, but not at the transcription level. Taken together, it was hypothesized that when lin-4 RNAs base pair to the 3'-UTR of lin-14, a specific translational repression on the lin-14 gene occurred.[1],[3] In 2000, another small regulatory RNA, lethal-7 (let-7) was identified. It was initially observed in the heterochronic pathway of C. elegans that is responsible for encoding a ~ 22 regulatory RNA, and its mechanism is similar to lin-4 RNA. It plays an important role in the transition of the larval stage of C. elegans, in which it allows the parasite to be able to transform from late-larval to the adult stage. Since its discovery, homologs of the let- 7 gene and even let- 7 RNA itself have been observed in other species such as fish, mice, and humans.[1],[13],[16] Later, these single-stranded RNAs, which are usually 19-24 nucleotides in length, were named miRNAs.[1],[15] In fact, miRNA is one of the many classes of small ncRNAs present in every location of the genome.[14] Mature miRNAs can silence the respective mRNAs through binding to their partial complementary sequence via an antisense mechanism.[1]

miRNAs regulate the posttranscriptional gene expression.[17] They can be seen in nonprotein-coding regions and even in protein-coding regions, and thus, they can be co-transcribed together with the host genes.[14] The formation of miRNAs is similar to the biogenesis of traditional mRNAs. After transcription, the miRNAs undergo capping, polyadenylating together with splicing to form long primary transcripts. However, in contrast to the mRNA, their active region is located within a ~70 nucleotide hairpin structure. In the early stage, RNA polymerase II situated in the nucleus initiates the formation of long primary transcripts, the pri-miRNAs that originate from the miRNA genes. MiRNA transcripts are known for having a complementary sequence within a characteristic transcript, thus allowing the RNA to be folded into a stem-loop or hairpin-like structure that can be further processed into a mature miRNA.[14],[18] This hairpin structure is later cleaved by Drosha and Dicer, the endonuclease enzymes, to generate a short 22-nucleotide ncRNA known as mature RNA that is similar to siRNA.[15] Eventually, this product is assembled into the RNA interference-effector complex, RNA-induced silencing complex (RISC).[1],[3],[12] The RISC consists of the Argonaute protein, trans-activation response RNA binding protein and Dicer. The Argonaute protein serves to cleave a nonguided strand through endonucleolytic hydrolysis, leaving behind a 5'-phosphate and a 3'-hydroxyl group at the end.[12],[18] The RISC is directed by miRNAs to down-regulate gene expressions by either one of two posttranscriptional mechanisms: cleavage of mRNA or translational repression. Consequently, this leads to decreased production of proteins. If the miRNA is highly complementary to the mRNA, a specific cleavage will occur. If no complementary site is present, the translational repression process will take over to suppress any productive translation.[1],[13],[15] [Figure 1] depicts the biogenesis of mature miRNA.
Figure 1: Biogenesis of mature microRNA. The microRNAs gene undergoes transcription by the RNA polymerase II to form the pri-microRNA that will be cleaved into pre-microRNA by Drosha. The pre-microRNA will be then exported out of the nucleus into the cytoplasm by the protein exportin-5. The pre-microRNA will be cleaved by Dicer, to form a MicroRNAs duplex consisting of a passenger strand and a mature microRNAs. The passenger strand will be degraded, whereas the mature microRNAs mediates gene-silencing processes by targeting specific messenger RNAs

Click here to view

  MicroRNAs and Diseases Top

MiRNAs are often discussed in relation to cancers either as oncogenes or their ability to down-regulate tumor suppressor genes by binding to 3'-UTR of the targeted mRNAs, destabilizing the mRNA, and leading to translational repression.[1],[4],[19],[20] Investigations on the differential expressions and patterns of miRNAs in cancers would provide a better understanding of their physiological and pathological roles in the human body, and enable the potential identification of therapeutic targets for various cancers.[1],[13],[14] In the past, microRNAs of the let-7 family have been associated with lung, ovary, cervical, urothelial, and breast cancers. For instance, let-7g was identified on 3p21, a region known to be involved in lung cancers. Further, an in vitro study showed that let-7 decreases the proliferation and stops cells in the G1-S transition, and is, therefore, acting as a tumor suppressor gene.[1] Moreover, let-7 has also been shown to reduce the expression of High Mobility Group AT-Hook 2, an oncogenic high-mobility group protein, and prevent differentiation of breast cancers as well as lung cancers.[1],[21] Decreased expressions of the let-7 family have also been associated with the overexpression of RAS oncogene, leading to a decreased survival rate in patients with nonsmall cell lung carcinoma.[22] In contrast, increased expressions of certain oncogenic miRNAs have been related to increased tumor growth, enhanced chemo-resistance, and down-regulation of apoptosis. For example, miR-21 has been found to be increased in glioblastoma multiforme (GBM) and detected at high levels in aggressive cancers.[1],[19],[22]

Recent studies have revealed that the miRNA-331 family members, namely, miRNA-331, miRNA-331-3p, and miRNA-331-5p, are associated with the pathology of some cancers, including colorectal cancer (CRC), leukemia, hepatocellular carcinoma (HCC), prostate cancer (PCa), pancreatic cancer, breast cancer, melanoma, and lung cancer. Therefore, it is important to have a good understanding about how the miRNA-331 family regulates the pathogeneses of these cancers. Hence, in this review, we discuss the pathological and physiological roles of the miRNA-331 family. Understanding how these miRNAs regulate the gene expression levels of their targets and their involvement in cancers may lead to better therapeutic strategies to treat cancers.


MiRNA-331 or miR-331 is a miRNA encoded by a gene located at the chromosomal position of 12q22.[23],[24],[25] It is known to be involved in solid tumors such as colorectal, leukemia, hepatocellular, and lung carcinoma.[26],[27],[28],[29],[30] To date, over 20 studies have reported altered expression levels of miRNAs in CRC. A previous microarray study reported that the expression of miRNAs in CRC was significantly different from that in nonneoplastic tissue.[31] Due to the possible involvement of miR-331 in CRC, Kanaan et al. proposed that it might be a potential biomarker which could be used to distinguish adenomas from CRC.[28]

MiR-331 has also been reported in studies of acute lymphocytic leukemia, chronic myeloid leukemia, and acute myeloid leukemia (AML).[26],[27] The miRNA has also been found to be involved in the down-regulation of suppressor of cytokine signaling, leading to increased cell proliferation.[27] Butrym et al. found that miR-331 was overexpressed in AML patients and that this overexpression was associated with a low-survival rate and also a poor response to chemotherapy. On the other hand, the miR-331 expression level was decreased in patients who had successful therapy, indicating that miR-331 is probably pro-oncogenic in nature.[26]

Another study showed that miR-331 was up-regulated in rat HCC.[30] This miRNA was also involved in lung adenocarcinoma (LUAD). It has also been reported that miR-331 might be useful as an independent prognostic marker in predicting the survival of LUAD patients for up to 5 years, regardless of the smoking history of the patients. The miRNA enables identification of those who are more prone toward the recurrence of LUAD. However, this study was limited by not taking into consideration adjuvant therapy received by the patients,[29] and adjuvant therapy might have altered the miRNA expression and interfered with the outcome of the study. Hence, it is advisable that any future studies should include the detailed clinical history of the patients. Sierzega et al. also demonstrated that miR-331 was overexpressed in gastric cancer, and that it was detected at a higher level in peripheral blood compared to the primary tumor vein, suggesting a localized alteration in miR-331 expression level in the tumor.[32]

A recent study also reported that, miR-331 was overexpressed in malignant breast tumors. Further analysis also revealed that the level of miR-331 might provide valuable information for the differential diagnosis of benign and malignant breast tumors.[33] In addition, another study also found that miR-331 was underexpressed in melanoma, and the overexpression of miR-331 has been reported to inhibit cell proliferation and invasion, probably by targeting AEG-1 and regulating the phosphatase and tensin homolog/protein kinase B (AKT) signaling pathway.[34]


MiR-331-3p is a member of the miRNA-331 family, with a length of around 21 nucleotides.[25] MiR-331-3p has been shown to be involved in cancers such as PCa, cervical cancer, glioblastoma, CRC, and HCC.[32],[35],[36],[37],[38],[39],[40],[41],[42]

PCa is the adenocarcinoma of prostate that is caused by a genetic mutation that activates the oncogenic phosphoinositide 3-kinase (PI3K)/Akt signaling pathway.[35] The overexpression of Erb-B2 receptor tyrosine kinase 2 (ERBB-2), commonly referred to as human epidermal growth factor receptor 2 (HER-2 or HER-2/neu), can lead to the activation of the PI3K/Akt pathway which triggers androgen receptor signaling in hormone-independent PCa. In 2009, Wang et al. demonstrated that miR-331-3p could induce apoptosis in PCa cells leading to growth arrest.[36] Similarly, Epis et al. demonstrated that miR-331-3p acts as a tumor suppressor by down-regulating the expression of ERBB-2 in PCa.[37] They proposed that the tumor-suppressing effects of miR-331-3p in PCa are associated with deoxyhypusine hydroxylase (DOHH) and eukaryotic translation initiation factor (eIF5A). DOHH is an enzyme responsible for catalyzing eIF5A and cell growth, and it has been found to be overexpressed in several PCa cell lines. It is likely that the overexpression of miR-331-3P in PCa cells decreases the expression of DOHH, and hence, stops cell proliferation.[22]

MiR-331-3p has been found to down-regulate HER-2 in breast cancer cells.[38] In addition, miR-331-3p has also been associated with gastric cancer. A long ncRNA, Hox transcript antisense intergenic RNA (HOTAIR) was shown to be up-regulated in gastric cancer in one study, and when miR-331-3p was added to the cancer cells, it was found that the expression level of HOTAIR was greatly reduced. In addition, results from a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed that gastric cancer cells transfected with miR-331-3p suffered from growth retardation, suggesting that miR-331-3p was antiproliferative to the cancer cells.[39] In another study, miRNA-331-3p was found to be involved in PCa and glioblastoma by regulating the expressions of epidermal growth factor receptor and HER-2 via reducing Akt activity.[18] MiR-331-3p has also been demonstrated to affect GBM by inhibiting the expression of neuropilin 2 (NRP-2), a receptor responsible for tumorigenesis, and that this can lead to decreased GBM cell proliferation.[19],[40] Similarly, the overexpression of miR-331-3p has been shown to suppress NRP-2 in cervical cancer cells, leading to the G2/M phase arrest followed by apoptosis.[41] Zhao et al. showed that miR-331-3p also participates in CRC. In addition, when miR-331-3p down-regulates HER-2 in colon cancer cells, it deactivates PI3/Akt as well as extracellular signal-regulated kinase 1/2 signaling pathways, thus acting as a tumor suppressor.[42]

MiR-331-3p has also been observed to play a role in HCC. According to an experiment performed at the Third People's Hospital of Nantong City, the level of miR-331-3p detected in the serum of HCC patients was significantly higher than that in control and benign groups, indicating its potential as a cancer biomarker.[43] Cao et al. suggested that the overexpression of miR-331-3p can actually lead to liver cancer cell proliferation and metastasis because miR-331-3p can target the Pleckstrin homology domain and the leucine-rich repeat protein phosphatase that is responsible for the proliferation and metastasis of cancer cells. They also found that miR-331-3p is probably overexpressed in the presence of hepatitis B virus (HBV). MiR-331-3p works through targeting the inhibitor of the growth 5 (ING5) gene which is a tumor suppressor gene. Their study showed that HBV probably upregulates the expression of miR-331-3p, subsequently inhibiting the ING5 gene. However, the findings were not conclusive, as the action of miR-331-3p on ING5 may be triggered by not only HBV but also by more yet unidentified factors.[44] Hence, more studies are still required to have a better understanding of the mode of action of miR-331-3p. [Figure 2] summarizes the molecular network in which miR-331-3p is critically involved in cancers.
Figure 2: Molecular network in which miR-331-3p is critically involved in various cancers. Overexpression of human epidermal growth factor receptor 2 is associated with breast cancer cell growth. It also leads to the activation of phosphoinositide 3-kinase/protein kinase B pathway and increased level of neuropilin which promotes the growth of prostate, colorectal and cervical cancers as well as glioblastoma. MiR-331-3p inhibits the growth of the cancer cells by inhibiting the expressions of human epidermal growth factor receptor 2 and neuropilin 2. Deoxyhypusine hydroxylase catalyzes eukaryotic translation initiation factor that is responsible for prostate cancer cell growth. Inhibition of deoxyhypusine hydroxylase by miR-331-3p stops the prostate cancer cell proliferation. MiR-331-3p inhibits gastric cancer growth by downregulating Hox transcript antisense intergenic RNA

Click here to view

A very recent study also revealed an association between miR-331-3p and pancreatic cancer. In that study, miR-331-3p was found to be tumor-promoting by targeting the gene of suppression of tumorigenicity 7 like, of which the gene sequence is highly similar to the ST7 tumor suppressor gene located at the chromosome 7q31 region, in pancreatic cancer cells.[45]


MiR-331-5p is also a member of the miR-331 family, with a length of around 22 nucleotides.[25] Its association with cancer was first mentioned in leukemia. It has been reported that the down-regulation of miR-331-5p is related to the overexpression of P-glycoprotein that can lead to anti-cancer drug resistance to doxorubicin.[46],[47] While the level of miR-331-5p is normally lower in cancer relapse patients with lymphocytic and myeloid leukemia, the overexpression of the miRNA has actually been shown to have a protective role by increasing drug sensitivity of the leukemic cells, thus inhibiting cancer drug resistance and preventing cancer relapse.[47]

Recently, Zhan et al. demonstrated the involvement of miR-331-5p in lung cancer.[48] It has also been found that miR-331-5p regulates the mitogen-activated protein kinase (MAPK) pathway that is responsible for tumor invasion, and also that it targets transforming growth factor beta 2 that is responsible for the metastasis of lung cancer. The role of miR-331-5p in nonsmall cell lung cancer was also confirmed in one study, in which circular RNA circ_0001649 was found to act as a sponge for miR-331-5p to inhibit the progression of nonsmall cell lung cancer.[49] When administered with curcumin or diferuloylmethane, a natural compound extracted from the spice turmeric (Curcuma longa) that is supposed to be chemopreventive agent in various types of cancer, it was found that the MAPK pathway was down-regulated.[50],[51] However, due to limited available information, the effects of curcumin in the regulation of miR-331-5p are still remain unknown, and thus, there is a need for further detailed studies.[50]

Apart from its association with cancers, miR-331-5p was also mentioned in a study about Parkinson's disease (PD). In that study, miR-331-5p was found to be a possible biomarker for PD. The study identified 384 miRNAs in the sera of PD patients and found that the expression of miR-331-5p was 21-fold higher in the patients than in the healthy controls. By using bioinformatics tools for gene analysis, it was predicted that the genes involved had the target sites of miR-331-5p in the 3'-UTR. Due to the limited number of patients in the study, the pathological roles of miR-331-5p remain elusive. Future studies should include a larger number of patients, preferably in different stages of PD. More studies are also needed to fully understand its mechanisms of action as well as its physiological or pathological roles.[52]

  Conclusion Top

In summary, the miRNA-331 family, including miRNA-331, miRNA-331-3p, and miRNA-331-5p, have been widely researched in cancer studies. MiRNA-331 has been shown to be involved and overexpressed in colorectal, leukemia, hepatocellular and lung carcinomas, whereas miRNA-331-3p has been shown to be involved in PCa, cervical cancer, glioblastoma, CRC, and HCC. Moreover, miRNA-331-5p has been associated with leukemia and lung cancer, as well as PD. Given that this family of miRNAs is involved in many types of cancers, its role in the pathogenesis and pathology of cancers should be further investigated.


The authors thank Ms. Pei Ling Yeo for her assistance in the project.

Financial support and sponsorship

The present study was supported by the Ministry of Higher Education, Malaysia (grant no. FRGS/2/2014/SKK01/MUSM/03/1).

Conflicts of interest

There are no conflicts of interest.

  References Top

Slack FJ. MicroRNAs in Development and Cancer. London, UK: Imperial College Press; 2011.  Back to cited text no. 1
Pachnis V, Brannan CI, Tilghman SM. The structure and expression of a novel gene activated in early mouse embryogenesis. EMBO J 1988;7:673-81.  Back to cited text no. 2
Bartel DP. MicroRNAs: Genomics, biogenesis, mechanism, and function. Cell 2004;116:281-97.  Back to cited text no. 3
Mattick JS. The genetic signatures of noncoding RNAs. PLoS Genet 2009;5:e1000459.  Back to cited text no. 4
Brown CJ, Ballabio A, Rupert JL, Lafreniere RG, Grompe M, Tonlorenzi R, et al. Agene from the region of the human X inactivation centre is expressed exclusively from the inactive X chromosome. Nature 1991;349:38-44.  Back to cited text no. 5
Djebali S, Davis CA, Merkel A, Dobin A, Lassmann T, Mortazavi A, et al. Landscape of transcription in human cells. Nature 2012;489:101-8.  Back to cited text no. 6
Thorsen SB, Obad S, Jensen NF, Stenvang J, Kauppinen S. The therapeutic potential of microRNAs in cancer. Cancer J 2012;18:275-84.  Back to cited text no. 7
Fabian MR, Sonenberg N, Filipowicz W. Regulation of mRNA translation and stability by microRNAs. Annu Rev Biochem 2010;79:351-79.  Back to cited text no. 8
Garzon R, Marcucci G, Croce CM. Targeting microRNAs in cancer: Rationale, strategies and challenges. Nat Rev Drug Discov 2010;9:775-89.  Back to cited text no. 9
van Kouwenhove M, Kedde M, Agami R. MicroRNA regulation by RNA-binding proteins and its implications for cancer. Nat Rev Cancer 2011;11:644-56.  Back to cited text no. 10
van Rooij E, Olson EN. MicroRNA therapeutics for cardiovascular disease: Opportunities and obstacles. Nat Rev Drug Discov 2012;11:860-72.  Back to cited text no. 11
Gomes AQ, Nolasco S, Soares H. Non-coding RNAs: Multi-tasking molecules in the cell. Int J Mol Sci 2013;14:16010-39.  Back to cited text no. 12
Sherbet GV. Therapeutic Strategies in Cancer Biology and Pathology. Waltham, USA: Elsevier; 2013.  Back to cited text no. 13
Neudecker V, Brodsky KS, Kreth S, Ginde AA, Eltzschig HK. Emerging roles for microRNAs in perioperative medicine. Anesthesiology 2016;124:489-506.  Back to cited text no. 14
Hammond SM. MicroRNA therapeutics: A new niche for antisense nucleic acids. Trends Mol Med 2006;12:99-101.  Back to cited text no. 15
Ambros V. MicroRNA pathways in flies and worms: Growth, death, fat, stress, and timing. Cell 2003;113:673-6.  Back to cited text no. 16
Vlachos IS, Paraskevopoulou MD, Karagkouni D, Georgakilas G, Vergoulis T, Kanellos I, et al. DIANA-tarBase v7.0: Indexing more than half a million experimentally supported miRNA:mRNA interactions. Nucleic Acids Res 2015;43:D153-9.  Back to cited text no. 17
Gaur RK, Gafni Y, Sharma P, Gupta VK. RNAi Technology. Boca Raton, USA: CRC Press; 2011.  Back to cited text no. 18
Giles KM, Barker A, Zhang PM, Epis MR, Leedman PJ. MicroRNA regulation of growth factor receptor signaling in human cancer cells. Methods Mol Biol 2011;676:147-63.  Back to cited text no. 19
Pasquinelli AE. MicroRNAs and their targets: Recognition, regulation and an emerging reciprocal relationship. Nat Rev Genet 2012;13:271-82.  Back to cited text no. 20
Lee YS, Dutta A. The tumor suppressor microRNA let-7 represses the HMGA2 oncogene. Genes Dev 2007;21:1025-30.  Back to cited text no. 21
Epis MR, Giles KM, Kalinowski FC, Barker A, Cohen RJ, Leedman PJ. Regulation of expression of deoxyhypusine hydroxylase (DOHH), the enzyme that catalyzes the activation of eIF5A, by miR-331-3p and miR-642-5p in prostate cancer cells. J Biol Chem 2012;287:35251-9.  Back to cited text no. 22
National Center for Biotechnology Information. MIR331 microRNA 331 [Homo sapiens (human)]; 2018. Available from: https://www.ncbi.nlm.nih.gov/gene/442903. [Last accessed on 2018 Jun 13].  Back to cited text no. 23
HUGO Gene Nomenclature Committee (HGNC). Symbol Report: MIR331; 2018. Available from: http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=HGNC: 31772. [Last accessed on 2018 Jun 13].  Back to cited text no. 24
Atlas of Genetics and Cytogenetics in Oncology and Haematology. MIR331 (microRNA 331); 2018. Available from: http://www.atlasgeneticsoncology.org/Genes/GC_MIR331.html#LINKS. [Last accessed on 2018 Jun 13].  Back to cited text no. 25
Butrym A, Rybka J, Baczyńska D, Tukiendorf A, Kuliczkowski K, Mazur G. Expression of microRNA-331 can be used as a predictor for response to therapy and survival in acute myeloid leukemia patients. Biomark Med 2015;9:453-60.  Back to cited text no. 26
Zanette DL, Rivadavia F, Molfetta GA, Barbuzano FG, Proto-Siqueira R, Silva WA Jr., et al. MiRNA expression profiles in chronic lymphocytic and acute lymphocytic leukemia. Braz J Med Biol Res 2007;40:1435-40.  Back to cited text no. 27
Kanaan Z, Roberts H, Eichenberger MR, Billeter A, Ocheretner G, Pan J, et al. Aplasma microRNA panel for detection of colorectal adenomas: A step toward more precise screening for colorectal cancer. Ann Surg 2013;258:400-8.  Back to cited text no. 28
Li X, Shi Y, Yin Z, Xue X, Zhou B. An eight-miRNA signature as a potential biomarker for predicting survival in lung adenocarcinoma. J Transl Med 2014;12:159.  Back to cited text no. 29
Sukata T, Sumida K, Kushida M, Ogata K, Miyata K, Yabushita S, et al. Circulating microRNAs, possible indicators of progress of rat hepatocarcinogenesis from early stages. Toxicol Lett 2011;200:46-52.  Back to cited text no. 30
Schetter AJ, Okayama H, Harris CC. The role of microRNAs in colorectal cancer. Cancer J 2012;18:244-52.  Back to cited text no. 31
Sierzega M, Kaczor M, Kolodziejczyk P, Kulig J, Sanak M, Richter P. Evaluation of serum microRNA biomarkers for gastric cancer based on blood and tissue pools profiling: The importance of miR-21 and miR-331. Br J Cancer 2017;117:266-73.  Back to cited text no. 32
Papadopoulos EI, Papachristopoulou G, Ardavanis A, Scorilas A. A comprehensive clinicopathological evaluation of the differential expression of microRNA-331 in breast tumors and its diagnostic significance. Clin Biochem 2018;60:24-32.  Back to cited text no. 33
Chen L, Ma G, Cao X, An X, Liu X. MicroRNA-331 inhibits proliferation and invasion of melanoma cells by targeting astrocyte-elevated gene-1. Oncol Res 2018;26:1429-37.  Back to cited text no. 34
Kumar V, Abbas A, Aster J. Robbins Basic Pathology. 9th ed. Philadelphia, USA: Elsevier Saunders; 2013.  Back to cited text no. 35
Wang L, Tang H, Thayanithy V, Subramanian S, Oberg AL, Cunningham JM, et al. Gene networks and microRNAs implicated in aggressive prostate cancer. Cancer Res 2009;69:9490-7.  Back to cited text no. 36
Epis MR, Giles KM, Barker A, Kendrick TS, Leedman PJ. MiR-331-3p regulates ERBB-2 expression and androgen receptor signaling in prostate cancer. J Biol Chem 2009;284:24696-704.  Back to cited text no. 37
Leivonen SK, Sahlberg KK, Mäkelä R, Due EU, Kallioniemi O, Børresen-Dale AL, et al. High-throughput screens identify microRNAs essential for HER2 positive breast cancer cell growth. Mol Oncol 2014;8:93-104.  Back to cited text no. 38
Liu XH, Sun M, Nie FQ, Ge YB, Zhang EB, Yin DD, et al. Lnc RNA HOTAIR functions as a competing endogenous RNA to regulate HER2 expression by sponging miR-331-3p in gastric cancer. Mol Cancer 2014;13:92.  Back to cited text no. 39
Epis MR, Giles KM, Candy PA, Webster RJ, Leedman PJ. MiR-331-3p regulates expression of neuropilin-2 in glioblastoma. J Neurooncol 2014;116:67-75.  Back to cited text no. 40
Fujii T, Shimada K, Asano A, Tatsumi Y, Yamaguchi N, Yamazaki M, et al. MicroRNA-331-3p suppresses cervical cancer cell proliferation and E6/E7 expression by targeting NRP2. Int J Mol Sci 2016;17. pii: E1351.  Back to cited text no. 41
Zhao D, Sui Y, Zheng X. MiR-331-3p inhibits proliferation and promotes apoptosis by targeting HER2 through the PI3K/Akt and ERK1/2 pathways in colorectal cancer. Oncol Rep 2016;35:1075-82.  Back to cited text no. 42
Chen L, Chu F, Cao Y, Shao J, Wang F. Serum miR-182 and miR-331-3p as diagnostic and prognostic markers in patients with hepatocellular carcinoma. Tumour Biol 2015;36:7439-47.  Back to cited text no. 43
Cao Y, Chen J, Wang D, Peng H, Tan X, Xiong D, et al. Upregulated in hepatitis B virus-associated hepatocellular carcinoma cells, miR-331-3p promotes proliferation of hepatocellular carcinoma cells by targeting ING5. Oncotarget 2015;6:38093-106.  Back to cited text no. 44
Liu T, Song Z, Gai Y. Circular RNA circ_0001649 acts as a prognostic biomarker and inhibits NSCLC progression via sponging miR-331-3p and miR-338-5p. Biochem Biophys Res Commun 2018;503:1503-9.  Back to cited text no. 45
Toscano-Garibay JD, Aquino-Jarquin G. Regulation exerted by miRNAs in the promoter and UTR sequences: MDR1/P-gp expression as a particular case. DNA Cell Biol 2012;31:1358-64.  Back to cited text no. 46
Feng DD, Zhang H, Zhang P, Zheng YS, Zhang XJ, Han BW, et al. Down-regulated miR-331-5p and miR-27a are associated with chemotherapy resistance and relapse in leukaemia. J Cell Mol Med 2011;15:2164-75.  Back to cited text no. 47
Zhan JW, Jiao DM, Wang Y, Song J, Wu JH, Wu LJ, et al. Integrated microRNA and gene expression profiling reveals the crucial miRNAs in curcumin anti-lung cancer cell invasion. Thorac Cancer 2017;8:461-70.  Back to cited text no. 48
Chen X, Luo H, Li X, Tian X, Peng B, Liu S, et al. MiR-331-3p functions as an oncogene by targeting ST7L in pancreatic cancer. Carcinogenesis 2018;39:1006-15.  Back to cited text no. 49
Singh M, Singh N. Curcumin counteracts the proliferative effect of estradiol and induces apoptosis in cervical cancer cells. Mol Cell Biochem 2011;347:1-11.  Back to cited text no. 50
Li L, Braiteh FS, Kurzrock R. Liposome-encapsulated curcumin:In vitro and in vivo effects on proliferation, apoptosis, signaling, and angiogenesis. Cancer 2005;104:1322-31.  Back to cited text no. 51
Cardo LF, Coto E, de Mena L, Ribacoba R, Moris G, Menéndez M, et al. Profile of microRNAs in the plasma of Parkinson's disease patients and healthy controls. J Neurol 2013;260:1420-2.  Back to cited text no. 52


  [Figure 1], [Figure 2]

This article has been cited by
1 Prostate Cancer-Associated miRNAs in Saliva: First Steps to an Easily Accessible and Reliable Screening Tool
Christoph Luedemann, Jan-Ludwig Reinersmann, Claudia Klinger, Stephan Degener, Nici Markus Dreger, Stephan Roth, Michael Kaufmann, Andreas Savelsbergh
Biomolecules. 2022; 12(10): 1366
[Pubmed] | [DOI]
2 Potential targets and molecular mechanism of miR-331-3p in hepatocellular carcinoma identified by weighted gene coexpression network analysis
Qingjia Chi, Xinge Geng, Kang Xu, Chunli Wang, Han Zhao
Bioscience Reports. 2020; 40(6)
[Pubmed] | [DOI]


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this article
MicroRNAs and Di...
Article Figures

 Article Access Statistics
    PDF Downloaded453    
    Comments [Add]    
    Cited by others 2    

Recommend this journal