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Article Publish Status: FREE
Abstract Title:

Isoalantolactone induces intrinsic apoptosis through p53 signaling pathway in human lung squamous carcinoma cells.

Abstract Source:

PLoS One. 2017 ;12(8):e0181731. Epub 2017 Aug 4. PMID: 28777796

Abstract Author(s):

Chengyan Jin, Guangxin Zhang, Yifan Zhang, Peiyan Hua, Ge Song, Mei Sun, Xin Li, Ti Tong, Bingjin Li, Xingyi Zhang

Article Affiliation:

Chengyan Jin

Abstract:

Isoalantolactone has recently been revealed to induce apoptosis in several types of cancer. However, little is reported on its anti-tumor potential on human lung cancer. Our present study was designed to investigate its effects on human lung squamous carcinoma SK-MES-1 cells. We found that Isoalantolactone induced cellular and DNA morphological changes and decreased the viability of SK-MES-1 cells. It significantly inhibited the growth of SK-MES-1 cells through apoptosis in a dose-dependent manner via activation of p53. It also induced cell cycle arrest at G1 phase. It can down-regulate Bcl-2 and up-regulate Bax, to induce dissipation of mitochondrial membrane potential and generation of reactive oxygen species. Caspase-3 was also activated by Isoalantolactone, with the cleavage of poly (ADP-ribose) polymerase. Our results reveal that Isoalantolactone induces intrinsic apoptosis in SK-MES-1 cells through p53 signaling pathway, which suggests that Isoalantolactone could be a potential leading compound for future development of anti-lung cancer drugs.

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