Twist2 promotes kidney cancer cell proliferation and invasion via regulating ITGA6 and CD44 expression in the ECM-Receptor-Interaction pathway

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Abstract

Twist2 is a member of the basic helix-loop-helix (bHLH) family and plays a critical role in tumorigenesis. Growing evidence proves that Twist2 involves in tumor progression; however, the role of Twist2 in human kidney cancer and its underlying mechanisms remain unclear. RT-PCR and Western blot analysis were used to detect the expression of Twist2 in kidney cancer cells and tissues. Cell proliferation, cell cycle, apoptosis, migration and invasion assay was measured by the Cell Count Kit-8 (CCK8), flow cytometry, wound healing and transwell analysis, respectively. Gene set enrichment analysis (GSEA) was used to identify correlation of Twist2 with ECM-Receptor-Interaction pathway. In this report, we show that Twist2 up-regulated in human kidney cancer tissues compared with normal kidney tissues. Twist2 promotes cell proliferation, inhibits cell apoptosis, augments cell migration and invasion in human kidney cancer-derived cell in vitro, and promotes tumor growth in vivo. Moreover, we found that knockdown of Twist2 decreased the levels of ITGA6 and CD44 which contribute to cell migration and invasion correlated with ECM-Receptor-Interaction pathway. This result indicates Twist2 may promote migration and invasion of kidney cancer cells by regulating ITGA6 and CD44 expression. Therefore, our data demonstrated that Twist2 involves in kidney cancer progression. The identification of the role Twist2 on the migration and invasion of kidney cancer provides a potential appropriate treatment after radical nephrectomy to get a better prognosis that reducing recurrence.

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Zhang, H. jie, Tao, J., Sheng, L., Hu, X., Rong, R. ming, Xu, M., & Zhu, T. yu. (2016). Twist2 promotes kidney cancer cell proliferation and invasion via regulating ITGA6 and CD44 expression in the ECM-Receptor-Interaction pathway. Biomedicine and Pharmacotherapy, 81, 453–459. https://doi.org/10.1016/j.biopha.2016.02.042

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