Imipramine-induced Apoptosis and Metastasis Inhibition in Human Bladder Cancer T24 Cells Through EGFR/ERK/NF-κB Pathway Suppression

丙咪嗪通过抑制EGFR/ERK/NF-κB通路诱导人膀胱癌T24细胞凋亡并抑制其转移

阅读:1

Abstract

BACKGROUND/AIM: Bladder cancer is a prevalent malignancy, ranging from superficial forms to more aggressive types that invade the muscle and require extensive treatment. Imipramine, traditionally used as an antidepressant, has shown potential as an anti-cancer agent. MATERIALS AND METHODS: In this study, human bladder cancer T24 cells were treated with varying concentrations of imipramine to evaluate its cytotoxic and apoptotic effects. RESULTS: Imipramine induced cytotoxicity in a dose-dependent manner, significantly increasing apoptosis as shown by Annexin-V/PI staining and TUNEL assay. The drug also up-regulated cleaved caspase-3 and down-regulated the anti-apoptotic factor XIAP. Moreover, imipramine activated both extrinsic/intrinsic apoptotic pathways, evidenced by the increased expression of Fas, FasL, cleaved caspase-8, and cleaved caspase-9, along with mitochondrial dysfunction and ROS production. Imipramine inhibited the migration and invasion of bladder cancer cells, likely through the down-regulation of metastasis-related proteins and suppression of the EGFR/ERK/NF-[Formula: see text]B signaling pathway. CONCLUSION: Imipramine could be a promising therapeutic agent for bladder cancer.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。