PMID:
Onco Targets Ther. 2019 ;12:8751-8763. Epub 2019 Oct 23. PMID: 31749621
Abstract Title:
Se-EnrichedInhibits Cell Proliferation, Induces Cell Apoptosis, And Causes G2/M Phase Arrest In Human Non-Small Cell Lung Cancer Cells.
Abstract:
Background: The anticancer effects of cordyceps on various tumors have been reported. However, little is known about the role of selenium (Se)-enrichedin non-small cell lung cancer (NSCLC). In this study, the effects of Se-enrichedon cell proliferation, cell apoptosis and cell cycle in NSCLC cell line NCI-H292 and A549 were investigated.Methods: CCK-8 assay was used to determine the appropriate concentrations of Se-enrichedin NSCLC (namely NCI-H292 and A549) cells. Colony formation assay, flow cytometric and Hoechst 33342 staining assays, and flow cytometric analysis were separately employed to assess the effect of increased Se-enrichedon NSCLC cell viability, cell apoptosis and cell-cycle distribution. Finally, the qPCR and Western blot assays were, respectively, applied to evaluate the effects of Se-enrichedon the expression of pro-apoptotic member BAX and the anti-apoptotic member BCL-2, as well as of G2/M cell cycle regulatory proteins CDK1 and cyclin B1.Results: The concentration of Se-enrichedwas 0, 4, 8, 12 mg/mL for NCI-H292 cells, and 0, 12.5, 25, 50 mg/mL for A549 cells. NSCLC cells treated with increased Se-enrichedshowed the inhibited cell viability. Se-enrichedinduced NSCLC cell apoptosis in concentration-dependent manner. Consistently, Se-enricheddiminished the ratio of anti-apoptotic member BCL-2 and pro-apoptotic member BAX at mRNA and protein levels in NSCLC cells. The percentage in G2/M phase was increased in NSCLC cells treated with increased Se-enriched. Downregulation of G2/M cell cycle regulatory proteins CDK1 and cyclin B1 at mRNA and protein levels in NSCLC cells further confirmed the effects of Se-enrichedon cell cycle.Conclusion: This study demonstrated the inhibitory role of Se-enrichedin cell proliferation and its facilitating role in cell apoptosis and cell cycle in NSCLC cells, suggesting an alternative therapeutic strategy for NSCLC treatment.
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