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miR-483-3p suppresses the proliferation and progression of human triple negative breast cancer cells by targeting the HDAC8>oncogene

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  • Mohammad Nazir Menbari, Kurdistan University of Medical Sciences
  • ,
  • Karim Rahimi
  • Abbas Ahmadi, Kurdistan University of Medical Sciences
  • ,
  • Samira Mohammadi-Yeganeh, Shahid Beheshti University of Medical Sciences
  • ,
  • Anvar Elyasi, Kurdistan University of Medical Sciences
  • ,
  • Nikoo Darvishi, Kurdistan University of Medical Sciences
  • ,
  • Vahedeh Hosseini, Kurdistan University of Medical Sciences
  • ,
  • Mohammad Abdi, Kurdistan University of Medical Sciences

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.

OriginalsprogEngelsk
TidsskriftJournal of Cellular Physiology
Vol/bind235
Nummer3
Sider (fra-til)2631-2642
Antal sider12
ISSN0021-9541
DOI
StatusUdgivet - mar. 2020

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