Publisher： Spandidos Publications
E-ISSN： 1791-2431|35|2|833-840
ISSN： 1021-335X
Source： Oncology Reports, Vol.35, Iss.2, 2016-01, pp. : 833-840
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Abstract
We investigated the effects of isoalantolactone on cell growth inhibition and underlying cell death mechanisms in SKOV3 human ovarian cancer cells. The effects of isoalantolactone on cell proliferation and cell cycle were examined by EdU incorporation assay and DNA content assay. Western blotting was performed to determine the protein expression effects of isoalantolactone on cell cyclerelated proteins, autophagic regulators and PEA15. Autophagic vacuoles were observed by acridine orange staining. PEA15 knockdown by siRNA was used to confirm that PEA15 was involved in isoalantolactoneinduced autophagy of SKOV3 cells. Isoalantolactone inhibited the viability and proliferation of SKOV3 cells in a dose and timedependent fashion. Isoalantolactone induced cell cycle arrest at G2/M phase and decreased the expression of cell cyclerelated proteins cyclin B1 and CDK1 in SKOV3 cells. Accordingly, isoalantolactone also induced SKOV3 cell autophagy via accumulation of autophagic vacuoles in the cytoplasm, increased Beclin1 protein expression, and increased LC3 cleavage. Furthermore, we observed that isoalantolactoneinduced autophagy was through increased PEA15 expression and the phosphorylation of ERK, whereas less change was observed to autophagy on SKOV3 cells through PEA15 knockdown by siRNA. Isoalantolactoneinduced autophagic cell death was further confirmed by pretreatment with the autophagy inhibitor 3methyladenine (3MA). In conclusion, isoalantolactone induced cell cycle arrest and autophagy and inhibited cell proliferation of SKOV3 cells via the upregulated PEA15 expression and the phosphorylation of ERK.
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