Knockdown of TM9SF4 triggering ER stress exerts anti-growth effect on drug-resistant breast cancer cells
Refereed conference paper presented and published in conference proceedings



摘要Drug-resistance of chemotherapy is the leading cause of mortality in breast cancer patients. Understanding how drug-resistant cancer cell survival is of great importance for the breast cancer therapy. Here, we identified a key protein, TM9SF4, namely transmembrane 9 superfamily, isoform 4, which play vital role in drug-resistant breast cancer survival. TM9SF4 is significantly up-regulated in drug-resistant breast cancer cells MCF-7/ADM compared to its parental wildtype cell line MCF-7/WT. Knockdown of TM9SF4 using lenti-TM9SF4-shRNA dramatically decreased cell viability and induced cell death of MCF-7/ADM. Moreover, drug-resistant xenografts derived from animal model also showed a significantly reduced growth rate after the delivery of lenti-TM9SF4-shRNA. The underlying mechanism may be related to the triggering of ER stress, leading to unfolded protein response, which will induce apoptosis/necrosis, causing cell death. Our study provides TM9SF4 as a promising target for the overcoming of drug-resistance in clinical breast cancer therapy.
著者ZHU Yifei, YAO Xiaoqiang
會議名稱18th World Congress of Basic and Clinical Pharmacology
會議地點Kyoto International Conference Center, Kyoto, Japan

上次更新時間 2018-04-12 於 16:43