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MiR-646 prevents proliferation and progression of human breast cancer cell lines by suppressing HDAC2 expression

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  • Nikoo Darvishi, Kerman University of Medical Sciences
  • ,
  • Karim Rahimi
  • Kamran Mansouri, Medical Biology Research Center, Kermanshah University of Medical Sciences, Kermanshah University of Medical Sciences
  • ,
  • Fardin Fathi, Cellular and Molecular Research Center, Kurdistan University of Medical Sciences
  • ,
  • Mohammad Nazir Menbari, Kurdistan University of Medical Sciences
  • ,
  • Gholamabbas Mohammadi, Kerman University of Medical Sciences
  • ,
  • Mohammad Abdi, Kurdistan University of Medical Sciences

Background: Breast cancer is a type of cancer with a high incidence and mortality rate worldwide. Change in epigenetic mechanisms enhances cancer cell progression. Histon deacetylase 2 (HDAC2) was found to act as a potential oncogene in different malignancies. For better understanding the mechanisms related to breast cancer development, we investigated the role of HDAC2 in breast cancer and the inhibitory effect of miR-646 on this oncogene. Methods: A total of thirty cancerous tissues and 30 adjacent non-cancerous specimens and also three breast cancer cell lines were enrolled in the study. Quantitative reverse transcriptase PCR (qRT-PCR) was employed to detect the HDAC2 and miR-646 expression level in the studied samples. The biological roles of HDAC2 and miR-646 were investigated through manipulating the expression level of HDAC2 or miR-646 in breast cancer cells. Finally, we evaluated whether the HDAC2 is a direct target for miR-646. Results: In this study, we found HDAC2 is significantly upregulated in cancerous specimens and cell lines compared to non-cancerous tissues and normal cell line. On the other hand, miR-646 expression was decreased in clinical specimens and breast cancer cells compared to non-cancerous samples. Knocking out of the HDAC2 and overexpression of miR-646 inhibited breast cancer cell growth but promoted cell death, while untreated groups showed inverse results. Furthermore, we showed that in the breast cancer cells, miR-646 regulates the progression and proliferation by suppressing HDAC2. Conclusion: Taken together, our study identified a miR-646/HDAC2 regulatory function in the breast cancer development and introduced a therapeutically target for breast cancer.

OriginalsprogEngelsk
Artikelnummer101649
TidsskriftMolecular and Cellular Probes
Vol/bind53
ISSN0890-8508
DOI
StatusUdgivet - okt. 2020

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