Volume 24, Issue 5 (Iranian South Medical Journal 2021)
Iran South Med J 2021, 24(5): 439-453 |
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Ebrahimi S O, Reiisi S. MiR-6165 Dysregulation in Breast Cancer and Its Effect on Cell Proliferation and Migration. Iran South Med J 2021; 24 (5) :439-453
URL: http://ismj.bpums.ac.ir/article-1-1514-en.html
URL: http://ismj.bpums.ac.ir/article-1-1514-en.html
1- Department of Genetics, School of Basic Sciences, Shahrekord University, Shahrekord, Iran
2- Department of Genetics, School of Basic Sciences, Shahrekord University, Shahrekord, Iran , s.reiisi@ sku.ac.ir s.reiisi@yahoo.com
2- Department of Genetics, School of Basic Sciences, Shahrekord University, Shahrekord, Iran , s.reiisi@ sku.ac.ir s.reiisi@yahoo.com
Abstract: (1795 Views)
Background: ncRNAs have been identified as oncogenic drivers and tumor suppressors in any type of cancer. Although many classes of ncRNAs have been reported, most studies have been performed on microRNAs (miRNAs). miRNAs can regulate several target genes and affect important processes such as homeostasis, angiogenesis, cell proliferation, differentiation, and apoptosis. Located in the p75NTR gene, miR-6165 is known to induce apoptosis in colorectal cell lines, and one study proposed a tumor suppressive role in colorectal cancer. However, its mechanism of action in breast cancer is not completely understood yet. Therefore, this study aimed to consider the expression level and the effect of miR-6165 on the proliferation and migration in breast cancer.
Material and methods: Fifty tumor and adjacent non-tumor tissues were examined in the study. miR-6165 levels were evaluated by qPCR in breast cancer cell lines and tumor tissues. Pre-mir-6165 was cloned in the pEGFPN1 vector. Next, human breast cancer MCF7 cells were cultured and pre-miR-6165 vector was transfected to breast cancer line. The effects on cell proliferation and migration were investigated with MTT assay and scratch test, respectively. Bioinformatics analysis was performed through enrichment and hub genes finding for miRNA targets.
Results: miR-6165 was overexpressed in breast cancer tumor tissues and cell lines. High expression of miR-6165 was directly related to the metastasis. miR-6165 increased proliferation and migration in breast cancer cell line.
Conclusions: miR-6165 may function as an oncomir and increase the growth and migration of cells which may consequently serve as a therapeutic goal for breast cancer.
Material and methods: Fifty tumor and adjacent non-tumor tissues were examined in the study. miR-6165 levels were evaluated by qPCR in breast cancer cell lines and tumor tissues. Pre-mir-6165 was cloned in the pEGFPN1 vector. Next, human breast cancer MCF7 cells were cultured and pre-miR-6165 vector was transfected to breast cancer line. The effects on cell proliferation and migration were investigated with MTT assay and scratch test, respectively. Bioinformatics analysis was performed through enrichment and hub genes finding for miRNA targets.
Results: miR-6165 was overexpressed in breast cancer tumor tissues and cell lines. High expression of miR-6165 was directly related to the metastasis. miR-6165 increased proliferation and migration in breast cancer cell line.
Conclusions: miR-6165 may function as an oncomir and increase the growth and migration of cells which may consequently serve as a therapeutic goal for breast cancer.
Type of Study: Original |
Subject:
General
Received: 2021/11/28 | Accepted: 2021/10/30 | Published: 2021/10/30
Received: 2021/11/28 | Accepted: 2021/10/30 | Published: 2021/10/30
References
1. Ambros V. The Functions Of Animal MicroRNAs. Nature 2004; 431(7006): 350-5.
2. Baltimore D, Boldin MP, O'Connell RM, et al. MicroRNAs: New Regulators Of Immune Cell Development And Function. Nat Immunol 2008; 9(8): 839-45.
3. Chang TC, Wentzel EA, Kent OA, et al. Transactivation of miR-34a by p53 Broadly Influences Gene Expression And Promotes Apoptosis. Mol Cell 2007; 26(5): 745-52.
4. Calin GA, Cimmino A, Fabbri M, et al. MiR-15a and miR-16-1 Cluster Functions In Human Leukemia. Proc Natl Acad Sci USA 2008; 105(13): 5166-71.
5. Xiao C, Rajewsky K. MicroRNA Control In The Immune System: Basic Principles. Cell 2009; 136(1): 26-36.
6. Johnson SM, Grosshans H, Shingara J, et al. RAS Is Regulated By The let-7 MicroRNA Family. Cell 2005; 120(5): 635-47.
7. Chen C, Ridzon DA, Broomer AJ, et al. Real-Time Quantification Of MicroRNAs By Stem–Loop RT–PCR. Nucleic Acids Res 2005; 33(20): e179.
8. Esquela-Kerscher A, Slack FJ. Oncomirs—microRNAs With A Role In Cancer. Nat Rev Cancer 2006; 6(4): 259-69.
9. Calin GA, Croce CM. MicroRNA Signatures In Human Cancers. Nat Rev Cancer 2006; 6(11): 857-66.
10. Lu J, Getz G, Miska EA, et al. MicroRNA Expression Profiles Classify Human Cancers. Nature 2005; 435(7043): 834-8.
11. Hamam R, Ali AM, Alsaleh KA, et al. microRNA Expression Profiling On Individual Breast Cancer Patients Identifies Novel Panel Of Circulating Microrna For Early Detection. Sci Rep 2016; 6: 25997.
12. Jones SK, Merkel OM. Tackling Breast Cancer Chemoresistance With Nano-Formulated siRNA. Gene Ther 2016; 23(12): 821-8.
13. Perou CM, Sørlie T, Eisen MB, et al. Molecular Portraits Of Human Breast Tumours. Nature 2000; 406(6797): 747-52.
14. Coates AS, Winer EP, Goldhirsch A, et al. Tailoring Therapies—Improving The Management Of Early Breast Cancer: St Gallen International Expert Consensus On The Primary Therapy Of Early Breast Cancer 2015. Ann Oncol 2015; 26(8): 1533-46.
15. Gambari R, Brognara E, Spandidos DA, et al. Targeting oncomiRNAs And Mimicking Tumor Suppressor miRNAs: Νew Trends In The Development Of miRNA Therapeutic Strategies In Oncology (Review). Int J Oncol 2016; 49(1): 5-32.
16. Parsi S, Soltani BM, Hosseini E, et al. Experimental Verification Of A Predicted Intronic microRNA In Human NGFR Gene With A Potential Pro-Apoptotic Function. PLoS One 2012; 7(4): e35561.
17. Hassanlou M, Soltani BM, Mowla SJ. Expression and Function of hsa-miR-6165 In Human Cell Lines And During The NT2 Cell Neural Differentiation Process. J Mol Neurosci 2017; 63(2): 254-66.
18. Peterson SM, Thompson JA, Ufkin ML, et al. Common Features Of microRNA Target Prediction Tools. Front Genet 2014; 5: 23.
19. França GS, Vibranovski MD, Galante PA. Host Gene Constraints And Genomic Context Impact The Expression And Evolution Of Human microRNAs. Nat Commun 2016; 7: 11438.
20. Wiley SZ, Sriram K, Salmerón C, et al. GPR68: An Emerging Drug Target In Cancer. Int J Mol Sci 2019; 20(3): 559.
21. Sens-Abuázar C, E Ferreira EN, Osório CA, et al. Down-regulation of ANAPC13 and CLTCL1: Early Events In The Progression Of Preinvasive Ductal Carcinoma Of The Breast. Transl Oncol 2012; 5(2): 113-23.
22. Baracco EE, Pietrocola F, Buqué A, et al. Inhibition Of Formyl Peptide Receptor 1 Reduces The Efficacy Of Anticancer Chemotherapy Against Carcinogen-Induced Breast Cancer. Oncoimmunology 2016; 5(6): e1139275.
23. Yang M, Chen J, Su F, et al. Microvesicles Secreted By Macrophages Shuttle Invasion-Potentiating microRNAs Into Breast Cancer Cells. Mol Cancer 2011; 10: 117.
24. Garg AD, De Ruysscher D, Agostinis P. Immunological Metagene Signatures Derived From Immunogenic Cancer Cell Death Associate With Improved Survival Of Patients With Lung, Breast Or Ovarian Malignancies: A Large-Scale Meta-Analysis. Oncoimmunology 2016; 5(2): e1069938.
25. Wu H, Bi J, Peng Y, et al. Nuclear Receptor NR4A1 Is A Tumor Suppressor Down-Regulated In Triple-Negative Breast Cancer. Oncotarget 2017; 8(33): 54364-77.
26. Hung CS, Wang SC, Yen YT, et al. Hypermethylation of CCND2 in Lung and Breast Cancer Is a Potential Biomarker and Drug Target. Int J Mol Sci 2018; 19(10): 3096.
27. Hajigholami S, Vaise Malekshahi Z. Nano Packaged Diblock and Curcumin: a New Approach Inorder To Drug Resistance in Breast Cancer. Iran South Med J. 2017; 19(6): 951-61.
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