Abstract PO-024: Paclitaxel induced apoptosis through ROS production and eliminated cellular senescence in PC9-MET cells

Background: Paclitaxel is used as first-line and subsequent therapy for the treatment of various cancers. However, the mechanisms by which paclitaxel exerts its anticancer activity against non-small cell lung cancer (NSCLC) are not well understood. This study aimed to investigate paclitaxel's role in cell proliferation, apoptosis, and cellular senescence of PC9-MET (gefitinib-resistant) cells and reveal the underlying mechanisms. Methods: PC9-MET cells were treated with paclitaxel for 72 h and then evaluated by cell viability assay, Giemsa staining, DAPI staining, apoptosis assay, SA-β-Gal staining, ROS assay, TUNEL assay and western blotting. Results: Our results revealed that paclitaxel significantly reduced the viability of PC9-MET cells and induced morphological signs of apoptosis. The apoptotic effects of paclitaxel were observed by increased levels of cleaved caspase-3, cleaved caspase-9 and cleaved PARP. Additionally, paclitaxel increased ROS production, leading to DNA damage. Importantly, paclitaxel eliminated cellular senescence, which was observed by SA-β-Gal staining. Conclusion: In light of these findings, paclitaxel could be a promising agent for cancer treatment against human PC9-MET (gefitinib-resistant) cells.

Citation Format: Md Mohiuddin, Kazuo Kasahara. Paclitaxel induced apoptosis through ROS production and eliminated cellular senescence in PC9-MET cells [abstract]. In: Proceedings of the AACR Virtual Special Conference on Radiation Science and Medicine; 2021 Mar 2-3. Philadelphia (PA): AACR; Clin Cancer Res 2021;27(8_Suppl):Abstract nr PO-024.