MiR-646 prevents proliferation and progression of human breast cancer cell lines by suppressing HDAC2 expression. (October 2020)

• Record Type: Journal Article
• Authors: Darvishi, Nikoo; Rahimi, Karim; Mansouri, Kamran; Fathi, Fardin; Menbari, Mohammad-Nazir; Mohammadi, Gholamabbas; Abdi, Mohammad
• Is Part Of: Molecular and cellular probes. Volume 53(2020)
• Publication Date: 2020-10
• Subjects: Breast cancer -- Cancer progression -- HDAC2 -- miR-646; Molecular probes -- Diagnostic use -- Periodicals; Pathology, Cellular -- Technique -- Periodicals; Cell Biology -- Periodicals; Molecular Biology -- Periodicals; Sondes moléculaires -- Utilisation diagnostique -- Périodiques; Cytopathologie -- Technique -- Périodiques; 572
• DOI: 10.1016/j.mcp.2020.101649
• Languages: English
• ISSNs: 0890-8508

Abstract

Abstract: 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. Highlights: MiR-646 expression was found down-regulated in breast cancer. We explored the tumour suppressive role of miR-646 in breast cancer. HDAC2 was reported to function as oncogene in breast cancer. HDAC2 was a direct target of miR-646 in breast cancer.