Open AccessIsoalantolactone induces intrinsic apoptosis through p53 signaling pathway in human lung squamous carcinoma cells
Author(s) -
Chengyan Jin,
Guangxin Zhang,
Yifan Zhang,
Peiyan Hua,
Ge Song,
Mei Sun,
Xin Li,
Ti Tong,
Bingjin Li,
Xingyi Zhang
Publication year - 2017
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0181731
Subject(s) - apoptosis , squamous carcinoma , reactive oxygen species , biology , microbiology and biotechnology , poly adp ribose polymerase , cell cycle , dna damage , cancer cell , signal transduction , mitochondrion , lung cancer , cancer research , viability assay , cancer , carcinoma , dna , biochemistry , polymerase , medicine , pathology , genetics
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.