Article ID Journal Published Year Pages File Type
1375832 Carbohydrate Polymers 2014 7 Pages PDF
Abstract

•We proved that PN50G can induce apoptosis in lung cancer cells for the first time.•PN50G inhibited the growth, metabolism and proliferation of A549 cells.•PN50G may trigger apoptosis via the mitochondria-dependent pathway.

Polysaccharides derived from edible fungi inhibit the proliferation of tumor cells. In this study, we investigated the effects of a polysaccharide (PN50G) from Pleurotus nebrodensis on A549 cell proliferation and apoptosis. MTT assay showed that PN50G induced apoptosis in the A549 cells in a dose-dependent. However, PN50G did not affect the proliferation viability of human fetal lung fibroblast cells MRC-5. Scanning electro microscopy (SEM) results indicate that PN50G induced a typical apoptotic morphological feature in A549. DNA accumulation and fragmentation were determined by acridine orange/ethidium bromide (AO/EB) staining. Flow cytometric analysis demonstrated that PN50G caused A549 cell apoptosis via cell arrest at the S phase. PN50G also extended the comet tail length in single-cell gel electrophoresis and disrupted the mitochondrial membrane potential as determined by Rdamine-123 staining. Further analysis by qRT-PCR showed that the expression of caspase-3 and caspase-9 mRNA increased. These findings suggest that PN50G can inhibit A549 cell proliferation and induce apoptosis mainly by activating the intrinsic mitochondrial pathway.

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