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Mir-483-3P Suppresses the Proliferation and Progression of Human Triple Negative Breast Cancer Cells by Targeting the Hdac8>Oncogene Publisher Pubmed



Menbari MN1 ; Rahimi K2, 3 ; Ahmadi A1 ; Mohammadiyeganeh S4, 5 ; Elyasi A6 ; Darvishi N1 ; Hosseini V1 ; Abdi M1, 7
Authors
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Authors Affiliations
  1. 1. Cellular and Molecular Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran
  2. 2. Department of Molecular Biology and Genetics-Gene Expression and Gene Medicine, Aarhus University, Aarhus, Denmark
  3. 3. Interdisciplinary Nanoscience Center, Aarhus University, Aarhus, Denmark
  4. 4. Medical Nanotechnology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  5. 5. Department of Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  6. 6. Department of Surgery, Faculty of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran
  7. 7. Department of Clinical Biochemistry, Faculty of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran

Source: Journal of Cellular Physiology Published:2020


Abstract

Triple negative breast cancer (TNBC) is a heterogeneous subclass of breast cancer (BC) distinguished by lack of hormone receptor expression. It is highly aggressive and difficult to treat with traditional chemotherapeutic regimens. Targeted-therapy using microRNAs (miR) has recently been proposed to improve the treatment of TNBC in the early stages. Here, we explore the roles of miR-483-3p/HDAC8 HDAC8 premiR-vector on tumorigenicity in TNBC patients. Clinical TNBC specimens and three BC cell lines were prepared. miR-483-3p and expression levels were measured using quantitative real-time polymerase chain reaction. Cell cycle progression was assessed by a flow-cytometry method. We also investigated cell proliferation by 3-2, 5-diphenyl tetrazolium bromide assay and colony formation assay. We used a to overexpress miR-483-3p, and a HDAC8-KO-vector for knocking out the endogenous production of HDAC8. Our data showed significant downregulation of miR-483-3p expression in TNBC clinical and cell line samples. The HDAC8 was also upregulated in both tissue specimens and BC cell lines. We found that increased levels of endogenous miR-483-3p affects tumorigenecity of MDA-MB-231. Downregulation of HDAC8 using the KO-vector showed the same pattern. Our results revealed that the miR-483-3p suppresses cellular proliferation and progression in TNBC cell lines via targeting HDAC8. Overall, our outcomes demonstrated the role of miR-483-3p as a tumor suppressor in TNBC and showed the possible mechanism via HDAC8. In addition, targeted treatment of TNBC with miR-483-3p might be considered in the future. © 2019 Wiley Periodicals, Inc.