A benzochalcone derivative synchronously induces apoptosis and ferroptosis in pancreatic cancer cells

被引:3
作者
Guan, Xiaoqing [1 ,2 ]
Zhao, Bing [1 ]
Guan, Xiaodan [1 ]
Dong, Jinyun [1 ]
Ying, Jieer [1 ,2 ]
机构
[1] Chinese Acad Sci, Zhejiang Canc Hosp, Hangzhou Inst Med HIM, Hangzhou, Zhejiang, Peoples R China
[2] Key Lab Prevent Diag & Therapy Upper Gastrointesti, Hangzhou, Zhejiang, Peoples R China
关键词
Pancreatic cancer; Therapeutic agent; Apoptosis; Ferroptosis; PLAC8; GEMCITABINE; ERLOTINIB;
D O I
10.7717/peerj.16291
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Background. Pancreatic cancer is a highly aggressive and lethal disease with limited treatment options. In this study, we investigated the potential therapeutic effects of compound KL-6 on pancreatic cancer cells. Methods. The study involved assessing the inhibitory effects of KL-6 on cell proliferation, clonogenic potential, cell cycle progression, apoptosis, migration, and invasion. Additionally, we examined the action mechanism of KL-6 by RNA-seq and bioinformatic analysis and validated by qRT-PCR and western blot in pancreatic cancer cells. Results. Our results demonstrated that KL-6 effectively inhibited the growth of pancreatic cancer cells in a dose-dependent manner. It induced G2/M phase cell cycle arrest and apoptosis, disrupting the cell cycle progression and promoting cell death. KL-6 also exhibited inhibitory effects on cell migration and invasion, suggesting its potential to suppress the metastatic properties of pancreatic cancer cells. Furthermore, KL-6 modulated the expression of genes involved in various cancer-related pathways including apoptosis and ferroptosis. Conclusion. These findings collectively support the potential of KL-6 as a promising therapeutic option for pancreatic cancer treatment. Further research is needed to fully understand the underlying mechanisms and evaluate the clinical efficacy of KL-6 in pancreatic cancer patients.
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页数:20
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