Knockdown of microRNA-29a Changes the Expression of Heat Shock Proteins in Breast Carcinoma MCF-7 Cells

• Published in: Oncology research 2016-01, Vol.23 (1-2), p.69-78
• Main Authors: Choghaei, Encieh, Khamisipour, Gholamreza, Falahati, Mojtaba, Naeimi, Behrooz, Mossahebi-Mohammadi, Majid, Tahmasebi, Rahim, Hasanpour, Mojtaba, Shamsian, Shakib, Hashemi, Zahra Sadat
• Format: Article
• Language: English
• Subjects: Antineoplastic Agents, Phytogenic - pharmacology; Breast Cancer; Breast Neoplasms - genetics; Breast Neoplasms - metabolism; Breast Neoplasms - pathology; Cell Survival; Female; Gene Expression; Gene Expression Regulation, Neoplastic; Gene Knockdown Techniques; Heat Shock Proteins (hsps); Heat-Shock Proteins - genetics; Heat-Shock Proteins - metabolism; Humans; MCF-7 Cells; MicroRNAs - genetics; MicroRNAs - metabolism; Mir-29a; Paclitaxel - pharmacology; RNA Interference
• ISSN: 0965-0407; 1555-3906
• DOI: 10.3727/096504015X14478843952906

Breast cancer is the most commonly occurring cancer among women. MicroRNAs as noncoding small RNA molecules play pivotal roles in cancer-related biological processes. Increased levels of microRNA-29a in the serum of breast cancer patients have been reported. Since heat shock proteins (HSPs) play important roles in cell events, the quantitative fluctuations in their cellular levels could be deemed as key indicators of how the exerted treatment alters cell behavior. In this regard, using an antisense small RNA, we attempted to investigate the effects of miR-29a knockdown on the expression of HSPs genes in the MCF-7 breast cancer cell line. MCF-7 cells were cultured in high-glucose Dulbecco's modified Eagle's medium with 10% FBS. Studied cells were subdivided into five groups: treated with scramble, anti-miR-29a, anti-miR-29a + Taxol, Taxol, and control. Taxol was added 24 h post-anti-miR transfection and RNA extraction, and cDNA synthesis was done 48 h later. The changes in expression of HSP27, HSP40, HSP60, HSP70, and HSP90 were evaluated by real-time PCR. Our results revealed that inhibitors of microRNA-29a promote apoptosis through upregulation of HSP60 level and downregulation of HSP27, HSP40, HSP70, and HSP90 levels and could be contemplated as a compelling alternative for Taxol employment with similar effects and/or to sensitize cancer cells to chemotherapy with fewer side effects.