Quercetin inhibits breast cancer cell proliferation and survival by targeting Akt/mTOR/PTEN signaling pathway

Recently, natural compounds such as quercetin have gained an increasing amount of attention in treating breast cancer. However, the exact mechanisms responsible for the antiproliferative functions of quercetin are not completely understood. Therefore, we aimed to examine quercetin impacts on breast...

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Veröffentlicht in:Chemical biology & drug design 2024-06, Vol.103 (6), p.e14557-n/a
Hauptverfasser: Jiang, Ji, Yang, Yan, Wang, Fuhuan, Mao, Wei, Wang, Zhongjun, Liu, Zegang
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Sprache:eng
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Zusammenfassung:Recently, natural compounds such as quercetin have gained an increasing amount of attention in treating breast cancer. However, the exact mechanisms responsible for the antiproliferative functions of quercetin are not completely understood. Therefore, we aimed to examine quercetin impacts on breast cancer cell proliferation and survival and the involvement of PI3K/Akt/mTOR pathway. Breast cancer MDA‐MB‐231 and MCF‐7 cells were exposed to quercetin, and cell proliferation was assessed by MTT assay. ELISA was applied to evaluate cell apoptosis. The expression levels of apoptotic mediators such as caspase‐3, Bcl‐2, Bax and PI3K, Akt, mTOR, and PTEN were assessed via qRT‐PCR and western blot. We found that quercetin suppressed dose dependently cell growth capacity in MDA‐MB‐231 and MCF‐7 cells. In addition, quercetin treatment increase apoptosis in both cells lines via modulating the pro‐ and antiapoptotic markers. Quercetin upregulated PTEN and downregulated PI3K, Akt, and mTOR, hence suppressing this signaling pathway in cells. In conclusion, we showed antiproliferative and pro‐apoptotic function of quercetin in breast cancer cell lines, which is mediated by targeting and suppressing PI3K/Akt/mTOR signal transduction. The antiproliferative and pro‐apoptotic functions of quercetin in breast cancer cell lines are mediated by targeting and suppressing PI3K/Akt/mTOR/PTEN signal transduction.
ISSN:1747-0277
1747-0285
DOI:10.1111/cbdd.14557