MiR-1268b confers chemosensitivity in breast cancer by targeting ERBB2-mediated PI3K-AKT pathway
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Wen-Jie Zhu1,2, Xu Chen1,2, Ya-Wen Wang1,2, Hai-Ting Liu1,2, Ran-Ran Ma1,2 and Peng Gao1,2
1Department of Pathology, Qilu Hospital, Shandong University, Jinan, P.R. China
2Department of Pathology, School of Medicine, Shandong University, Jinan, P.R. China
Peng Gao, email: firstname.lastname@example.org
Keywords: MiR-1268b, breast cancer, chemoresistance, ERBB2, PI3K-AKT
Received: April 13, 2017 Accepted: July 12, 2017 Published: August 09, 2017
Chemoresistance represents a major obstacle to effective therapy for breast cancer. Emerging evidences associated aberrantly expressed miRNAs with tumor development and chemoresistance. MiR-1268b has never been studied in any cancers before, and its roles in mediating tumor progression and drug resistance are still unclear. Selected from miRNA microarray and confirmed by real-time quantitative PCR (RT-qPCR), miR-1268b was found to be significantly upregulated in drug sensitive and ERBB2 negative tissues, as well as in breast cancer patients with low clinical stage. And miR-1268b had a higher expression in chemosensitive breast cancer cell lines, compared with the chemoresistant cell line. Moreover, the results revealed that miR-1268b induced breast cancer cell apoptosis and increased cell chemosensitivity. ERBB2 was demonstrated to be the target gene of miR-1268b by dual-luciferase reporter assays, western blot, and immunocytochemistry. Furthermore, PI3KCA, AKT, BCL2 in the ERBB2-PI3K-AKT signaling pathway were found to be downstream effectors of miR-1268b. In conclusion, miR-1268b increased chemosensitivity, at least in part, via modulation of PI3K-AKT pathway by targeting ERBB2. MiR-1268b may serve as a potential therapeutic target for patients with breast cancers.
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