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Selenite-induced autophagy antagonizes apoptosis in colorectal cancer cells in vitro and in vivo

In the present study, we aimed to investigate the relationship between autophagy and apoptosis in selenite-treated colorectal cancer (CRC) cells. The effects of selenite on HCT116 and SW480 cell apoptosis were investigated with an Annexin V/propidium iodide (PI) double staining kit by flow cytometry...

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Detalles Bibliográficos
Autores principales: YANG, YANG, LUO, HUI, HUI, KAIYUAN, CI, YALI, SHI, KEJIAN, CHEN, GE, SHI, LEI, XU, CAIMIN
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4750746/
https://www.ncbi.nlm.nih.gov/pubmed/26676801
http://dx.doi.org/10.3892/or.2015.4484
Descripción
Sumario:In the present study, we aimed to investigate the relationship between autophagy and apoptosis in selenite-treated colorectal cancer (CRC) cells. The effects of selenite on HCT116 and SW480 cell apoptosis were investigated with an Annexin V/propidium iodide (PI) double staining kit by flow cytometry. The punctate of LC3 protein following treatment with selenite was observed by a laser scanning confocal microscope and by transmission electron microscopy. Using western blot assays, we detected the apoptotic and autophagic markers in both CRC cells and mouse xenograft tumor models. We found that sodium selenite induced autophagy in the two CRC cell lines. Consistent with the in vitro results, we observed that the expression of autophagy marker LC3 was increased. Finally, we discovered that modulation of reactive oxygen species by MnTMPyP inhibited autophagy, while H(2)O(2) activated autophagy. These results help to elucidate the anticancer effect of selenium, providing further evidence to exploit novel anticancer drugs targeting selenium.