Chlorpromazine cooperatively induces apoptosis with tyrosine kinase inhibitors in EGFR-mutated lung cancer cell lines and restores the sensitivity to gefitinib in T790M-harboring resistant cells.

doi:10.1016/j.bbrc.2022.08.010

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Chlorpromazine cooperatively induces apoptosis with tyrosine kinase inhibitors in EGFR-mutated lung cancer cell lines and restores the sensitivity to gefitinib in T790M-harboring resistant cells.

Biochemical and biophysical research communications - 20 Oct 2022

Fujiwara Ryosuke, Taniguchi Yasuhiro, Rai Shinya, Iwata Yoshio, Fujii Aki, Fujimoto Ko, Kumode Takahiro, Serizawa Kentaro, Morita Yasuyoshi, Espinoza J Luis, Tanaka Hirokazu, Hanamoto Hitoshi, Matsumura Itaru

Abstract excerpt

We previously reported that the antipsychotic drug chlorpromazine (CPZ), which inhibits the formation of clathrin-coated vesicles (CCVs) essential for endocytosis and intracellular transport of receptor tyrosine kinase (RTK), inhibits the growth/survival of acute myeloid leukemia cells with mutated RTK (KIT D816V or FLT3-ITD) by perturbing the intracellular localization of these molecules. Here, we examined...

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Chlorpromazine cooperatively induces apoptosis with tyrosine kinase inhibitors in EGFR-mutated lung cancer cell lines and restores the sensitivity to gefitinib in T790M-harboring resistant cells.

Abstract excerpt

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