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Quercetin preferentially induces apoptosis in KRAS-mutant colorectal cancer cells via JNK signaling pathways.

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机构： [1]West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, P. R. China [2]Laboratory of Molecular and Translational Medicine, West China Second University Hospital, Sichuan University, Chengdu, P. R. China [3]Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, P. R. China

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关键词： apoptosis colorectal cancer JNK KRAS mutation quercetin

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Colorectal cancer (CRC) is the third most common type of cancer, and its incidence and mortality are markedly increasing worldwide. Oncogenic mutations of KRAS occur in up to 40% of CRC cases and pose a great challenge in the treatment of the disease. Quercetin is a dietary flavonoid that exerts anti-oxidant, anti-inflammatory, and anti-cancer properties. The current study investigated the anti-proliferative effect of quercetin on CRC cells harboring mutant or wild-type KRAS. The effect of quercetin on cell viability was investigated by MTT and colony formation assays, and apoptosis was detected using flow cytometry by labeling cells with Annexin V-FITC. The expression of the relevant proteins was examined by Western blotting. The data revealed that KRAS-mutant cells were more sensitive to quercetin-induced apoptosis than wild-type cells. Caspase activation was involved in quercetin-induced apoptosis. In addition, quercetin selectively activated the c-Jun N-terminal kinase (JNK) pathway in KRAS-mutant cells, while inhibition of phospho-JNK by SP600125 blocked quercetin-induced apoptosis. The results of the present study suggest that treatment with quercetin, a common flavonoid in plants, is potentially a useful strategy for the treatment of CRCs carrying KRAS mutations. © 2018 International Federation for Cell Biology.

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出版当年[2019]版：

大类 | 4 区生物学

小类 | 4 区细胞生物学

最新[2023]版：

大类 | 3 区生物学

小类 | 4 区细胞生物学

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第一作者机构： [1]West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, P. R. China

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