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Imipramine-induced Apoptosis and Metastasis Inhibition in Human Bladder Cancer T24 Cells Through EGFR/ERK/NF-κB
Wei-Shu Wang1,2, Yu-Chang Liu3,4, Tsai-Lin Lo5
1Department of Medicine, National Yang Ming Chiao Tung University Hospital, Yilan, Taiwan, R.O.C.
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.
