Background: The anticancer effects of cordyceps on various tumors have been reported. However, little is known about the role of selenium (Se)-enriched in non-small cell lung cancer (NSCLC). In this study, the effects of Se-enriched on 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-enriched in 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-enriched on 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-enriched on 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-enriched was 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-enriched showed the inhibited cell viability. Se-enriched induced NSCLC cell apoptosis in concentration-dependent manner. Consistently, Se-enriched diminished 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-enriched on cell cycle.
Conclusion: This study demonstrated the inhibitory role of Se-enriched in 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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http://dx.doi.org/10.2147/OTT.S217017 | DOI Listing |
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Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China.
Cancer-associated fibroblasts (CAFs) significantly influence tumor progression and therapeutic resistance in colorectal cancer (CRC). However, the distributions and functions of CAF subpopulations vary across the four consensus molecular subtypes (CMSs) of CRC. This study performed single-cell RNA and bulk RNA sequencing and revealed that myofibroblast-like CAFs (myCAFs), tumor-like CAFs (tCAFs), inflammatory CAFs (iCAFs), CXCL14CAFs, and MTCAFs are notably enriched in CMS4 compared with other CMSs of CRC.
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