抑制 RAS/ROCK 或 mTOR 對於人類尿路上皮癌的侵襲和轉移

Abstract

Recent literature has reported that urothelial carcinoma (UC) is with continuously rising of incidence worldwide. Among UC, bladder cancer is the most common cancer. The incidence of age have tended to be olderer. Currently side effects of cancer treatment of a relatively small targeted therapy other treatments.mTOR is important role in PI3K/AKTmTOR pathway. That mTOR inhibitor (Everolimus) could inhibit the growth of idiopathic bladder cancer.However,the effect is limited of mTOR inhibitor for bladder cancer. This study examined everolimus for the heterogeneous mechanisms of bladder cancer need to be clarified. The T24, HT1376 and HT1197 cells after treatment with everolimus, mTOR, NFκB, MMP and p-GSK were decreased,whereas T24,HT1376 and HT1197 cells treated with Y27632 (Ras/ROCK inhibitor) Ras/ROCK is not be inhibited, Y27632 attenuated the Ras and related proteins of TSGH cells,but not in T24, HT1376, HT1197 cells. Using Transwell assay, the T24, HT1376, HT1197 cells amount of migration exposed to Everolimus and TSGH cells migrated numbers treated with Y27632 were dose-dependently decreased respectively. Using ECIS assay, the T24, HT1376, HT1197 cells amount of wound healing exposed to Everolimus and TSGH cells wound healing exposed treated with Y27632 were dose-dependently decreased respectively. Our study revealed that four different cell lines from human urothelial cell carcinoma (UCC) are regulated by different signaling pathways. In the future, the target therapy through confirming the molecular change of cancer cell firstly might increase to suit the medicine to the illness in patients.