Imipramine induced G1/S phase arrest, whereas tropisetron, ketanserin, and cyproheptadine increased the sub-G1 cell population. Gene expression analysis revealed decreased Bcl-2 and PCNA levels and increased Bax expression.These findings suggest the potential of tropisetron, imipramine, ketanserin, and cyproheptadine as repurposed therapeutic agents for gastric cancer.
3 months ago
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • BAX (BCL2-associated X protein) • PCNA (Proliferating cell nuclear antigen) • SLC6A4 (Solute Carrier Family 6 Member 4)
These findings highlight the dual role of fascin in tumor cells and the tumor microenvironment (TME), and reinforce its potential as a biomarker for personalized TNBC therapies. Ongoing clinical trials, including HITCLIF, are exploring the efficacy of imipramine in patients with fascin-overexpressing cancers, paving the way for targeted treatment strategies.
Moreover, co-treatment with imipramine enhanced the cytotoxic effects of sorafenib, suggesting that targeting MVP-associated pathways may improve sorafenib response. Collectively, these findings offer mechanistic insight into how sorafenib modulates MVP release and supports the therapeutic potential of combining tyrosine kinase inhibitors with agents that disrupt MVP biogenesis in NSCLC.