PA-MSHA inhibits proliferation and induces apoptosis in human non-small cell lung cancer cell lines with different genotypes

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Abstract

The present study examined the potential of Pseudomonas aeruginosa-mannose sensitive hemagglutinin (PA-MSHA) to inhibit proliferation and induce apoptosis in non-small-cell lung cancer (NSCLC) cell lines. It also investigated its mechanisms of action in different genotypes of human NSCLC. A total of three NSCLC cell lines, PC-9, A549, and NCI-H1975, were treated with PA-MSHA at different concentrations. The anti-proliferative effect of PA-MSHA was evaluated using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell cycle distribution and apoptosis induced by the treatment were measured by flow cytometry (FCM) with Annexin V/propidium iodide staining. Western blotting was conducted to determine the expression level of apoptosis-associated proteins. PA-MSHA was demonstrated to exert a time-and concentration-dependent cytotoxic effect in PC-9, A549, and NCI-H1975 cells. The FCM indicated that all the different concentrations of PA-MSHA used in the present study induce apoptosis and cell cycle arrest of NSCLC cells. Treatment with PA-MSHA may exert anti-proliferative effects on NSCLC cells by affecting regulation of the cell cycle and inducing apoptosis that is mediated in part by an intrinsic apoptosis signaling pathway. These data suggest that PA-MSHA has the potential to inhibit proliferation and induce apoptosis in NSCLC cells. Furthermore, these data provide mechanistic details for the potential application of PA-MSHA-based therapeutic strategies for the treatment of different NSCLC genotypes. This present study suggests potential novel strategies to maximize effective therapeutic strategies targeting anti-epidermal growth factor receptor for future clinical trials.

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Zhao, X., Wu, X., Yu, W., Cai, X., Liu, Q., Fu, X., … Huang, Q. (2016). PA-MSHA inhibits proliferation and induces apoptosis in human non-small cell lung cancer cell lines with different genotypes. Molecular Medicine Reports, 14(6), 5369–5376. https://doi.org/10.3892/mmr.2016.5869

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