Vol 9: Trail Resistance Induces Epithelial-Mesenchymal Transition and Enhances Invasiveness by Suppressing PTEN via miR-221 in Breast Cancer.Report as inadecuate



 Vol 9: Trail Resistance Induces Epithelial-Mesenchymal Transition and Enhances Invasiveness by Suppressing PTEN via miR-221 in Breast Cancer.


Vol 9: Trail Resistance Induces Epithelial-Mesenchymal Transition and Enhances Invasiveness by Suppressing PTEN via miR-221 in Breast Cancer. - Download this document for free, or read online. Document in PDF available to download.

Download or read this book online for free in PDF: Vol 9: Trail Resistance Induces Epithelial-Mesenchymal Transition and Enhances Invasiveness by Suppressing PTEN via miR-221 in Breast Cancer.
This article is from PLoS ONE, volume 9.AbstractTumor necrosis factor-related apoptosis-inducing ligand TRAIL can selectively induce apoptosis of cancer cells and is verified effective to various cancers. However, a variety of breast cancer cell lines are resistant to TRAIL and the mechanisms of resistance are largely unknown. In our present experiment, we successfully utilized breast cancer cell line MDA-MB-231 to establish TRAIL-resistant cell line. We found resistance to TRAIL could induce epithelial-mesenchymal transition EMT and enhance invasiveness. We further demonstrated PTEN was down-regulated in TRAIL-resistant cells. Silencing miR-221, PTEN expression was up-regulated, the process of EMT could be reversed, and the ability of migration and invasion were correspondingly weakened. We also demonstrated knockdown of miR-221 could reverse resistance to TRAIL partially by targeting PTEN. Our findings suggest that resistance to TRAIL could induce EMT and enhance invasiveness by suppressing PTEN via miR-221. Re-expression of miR-221 or targeting PTEN might serve as potential therapeutic approaches for the treatment of Trail-resistant breast cancer.



Author: Wang, Haiji; Xu, Chunyuan; Kong, Xiaoli; Li, Xiaoyan; Kong, Xiangnan; Wang, Yu; Ding, Xia; Yang, Qifeng

Source: https://archive.org/







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