The Function Role of miR-181a in Chemosensitivity to Adriamycin by Targeting Bcl-2 in Low-Invasive Breast Cancer Cells

Autor: Ying Zhu, Jianzhong Wu, Shuchun Li, Rong Ma, Haixia Cao, Minghua Ji, Changwen Jing, Jinhai Tang
Jazyk: angličtina
Rok vydání: 2013
Předmět:
Zdroj: Cellular Physiology and Biochemistry, Vol 32, Iss 5, Pp 1225-1237 (2013)
Druh dokumentu: article
ISSN: 1015-8987
1421-9778
DOI: 10.1159/000354521
Popis: Objectives: miR-181a is involved in immunity, metabolism, tumor suppression or carcinogenesis reported by many other studies. However, its role in the development of chemosensitivity to adriamycin in low-invasive breast cancer cells remains unclear. The aim of this study is to define the function role of miR-181a in promoting the efficacy of adriamycin-based neoadjuvant chemotherapy. Methods: Cell survival analysis was detected by Cell Counting Kit-8 assay. Apoptotic cells were quantitatively detected using FITC Annexin V apoptosis Detection Kit I. Bcl-2 protein expression was measured by western blot. Luciferase reporter vector with the putative BCL-2 3' untranslated region (3'UTR) was constructed to explore whether BCL-2 was a direct target gene of miR-181a. Real-time PCR was performed to test the expression of miR-181a and Bcl-2 in the selected breast cancer tissue samples. Results: The down-regulation of miR-181a decreased adriamycin-induced apoptosis in MCF-7 cells. Transfected with miR-181a mimic in cells resulted in the decreased expression of Bcl-2. The alteration of miR-181a expression did not significantly affect the chemosensitivity to adriamycin in MCF-7 and MCF-7/ADR cells with genetic knockout of Bcl-2. miR-181a may suppress Bcl-2 expression by forming imperfect base pairing with the 3'UTR of Bcl-2 gene such that a negative relationship between miR-181a and Bcl-2 in MCF-7 and MCF-7/ADR cells is observed. Conclusions: At least in part, the detection of miR-181a may direct the clinical medication in patients with neoadjuvant chemotherapy because of miR-181a enhanced adriamycin-induced apoptosis via targeting Bcl-2.
Databáze: Directory of Open Access Journals
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