Bavachinin led to the induction of G2/M cell cycle arrest in non-small-cell lung cancer cells.

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PMID: Molecules. 2021 Aug 25 ;26(17). Epub 2021 Aug 25. PMID: 34500594 Abstract Title: Induction of G2/M Cell Cycle Arrest via p38/p21-Dependent Signaling Pathway Activation by Bavachinin in Non-Small-Cell Lung Cancer Cells. Abstract: Lung cancer is the most commonly diagnosed malignant cancer in the world. Non-small-cell lung cancer (NSCLC) is the major category of lung cancer. Although effective therapies have been administered, for improving the NSCLC patient's survival, the incident rate is still high. Therefore, searching for a good strategy for preventing NSCLC is urgent. Traditional Chinese medicine (TCM) are brilliant materials for cancer chemoprevention, because of their high biological safety and low cost. Bavachinin, which is an active flavanone ofL., possesses anti-inflammation, anti-angiogenesis, and anti-cancer activities. The present study's aim was to evaluate the anti-cancer activity of bavachinin on NSCLC, and its regulating molecular mechanisms. The results exhibited that a dose-dependent decrease in the cell viability and colony formation capacity of three NSCLC cell lines, by bavachinin, were through G2/M cell cycle arrest induction. Meanwhile, the expression of the G2/M cell cycle regulators, such as cyclin B, p-cdc2, p-cdc2, and p-wee1, was suppressed. With the dramatic up-regulation of the cyclin-dependent kinase inhibitor, p21, the expression and association of p21with the cyclin B/cdc2 complex was observed. Silencing the p21expression significantly rescued bavachinin-induced G2/M cell accumulation. Furthermore, the expression of p21mRNA was up-regulated in bavachinin-treated NSCLC cells. In addition, MAPK and AKT signaling were activated in bavachinin-added NSCLC cells. Interestingly, bavachinin-induced p21expression was repressed after restraint p38 MAPK activation. The inhibition of p38 MAPK activation reversed bavachinin-induced p21mRNA expression and G2/M cell cycle arrest. Collectively, bavachinin-induced G2/M cell cycle arrest was through the p38 MAPK-mediated p21-dependent signaling pathway in the NSCLC cells.
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