ArticleIn vivo (Athens, Greece)
Imipramine-induced Apoptosis and Metastasis Inhibition in Human Bladder Cancer T24 Cells Through EGFR/ERK/NF-κB Pathway Suppression.
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Identification of MYC co-expression gene: POLR3G is associated with cell senescence, immunotherapy, chemotherapy responses, and clinical prognosis in bladder cancer patients.Translational oncology · 2026Article
- Repurposing tricyclic drugs as cancer therapeutics: comparative analysis of antitumorigenic effects of chlorpromazine, amitriptyline and imipramine.Frontiers in oncology · 2026Article
- Magnolol Potentiates Sorafenib-induced Apoptosis and Inhibits Metastatic Signaling in Renal Carcinoma.In vivo (Athens, Greece)Article
- miR-124 Targets EGFR and Attenuates Growth and Invasion in Bladder Cancer Cells.In vivo (Athens, Greece)Article
- Lenvatinib Suppresses Colorectal Cancer Cell Growth, Migration, and InvasionIn vivo (Athens, Greece)Article
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Authors and funding
5 authors.
Funding
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Abstract
BACKGROUND/
aimBladder 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
methodsIn this study, human bladder cancer T24 cells were treated with varying concentrations of imipramine to evaluate its cytotoxic and apoptotic effects.
resultsImipramine 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.
conclusionImipramine could be a promising therapeutic agent for bladder cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.