miR-216b suppresses breast cancer growth and metastasis by targeting SDCBP

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• 作者：Samir Jana^a ; Suman Sengupta^a ; Subir Biswas^a ; Annesha Chatterjee^a ; Himansu Roy^b ; Arindam Bhattacharyya^a ; ^{arindam19@yahoo.com}
• 关键词：SDCBP ; miR-216b ; Breast cancer
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2017
• 出版时间：1 January 2017
• 年：2017
• 卷：482
• 期：1
• 页码：126-133
• 全文大小：1176 K
• 卷排序：482

文摘

Breast cancer is the most deadly cancer among women and the second leading cause of cancer death worldwide. Treatment effectiveness is complicated with tumor invasiveness/drug resistance. To tailor treatments more effectively to individual patients, it is important to define tumor growth and metastasis at molecular levels. SDCBP is highly overexpressed and associated with a strikingly poor prognosis in breast cancer. However the post transcriptional regulation of SDCBP overexpression remains to be an unexplored area. Our study reveals that miR-216b directly regulates SDCBP expression by binding to its 3′UTR region. miR-216b is a tumor suppressive miRNA and it is underexpressed during metastatic breast cancer. Consequently, overexpression of miR-216b resulted in decreased proliferation, migration and invasion in BC cell lines by modulating the expression of SDCBP. Inhibition of miR-216b divergent the tumor suppressive role by inducing the growth proliferation, migration and invasion in vitro. There is therefore a negative correlation between the expression of miR-216b and its target gene SDCBP in the BC tissue samples as well as cell lines. Simultaneous expression of miR-216b and SDCBP rescued the growth, migration and invasion effect suggesting that tumor suppressive action of miR-216b may be directly mediated by SDCBP. In summary, the study identifies miR-216b as a regulator of SDCBP expression in breast cancer which can potentially be targeted for developing newer therapies for the effective treatment of this killer disease.