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Isoalantolactone induces intrinsic apoptosis through p53 signaling pathway in human lung squamous carcinoma cells.
- Source :
-
PloS one [PLoS One] 2017 Aug 04; Vol. 12 (8), pp. e0181731. Date of Electronic Publication: 2017 Aug 04 (Print Publication: 2017). - Publication Year :
- 2017
-
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.
- Subjects :
- Carcinoma, Non-Small-Cell Lung drug therapy
Carcinoma, Non-Small-Cell Lung metabolism
Carcinoma, Squamous Cell drug therapy
Carcinoma, Squamous Cell metabolism
Caspases metabolism
Humans
Lung Neoplasms drug therapy
Lung Neoplasms metabolism
Membrane Potential, Mitochondrial drug effects
Reactive Oxygen Species metabolism
Signal Transduction drug effects
Tumor Cells, Cultured
Apoptosis drug effects
Carcinoma, Non-Small-Cell Lung pathology
Carcinoma, Squamous Cell pathology
Lung Neoplasms pathology
Sesquiterpenes pharmacology
Tumor Suppressor Protein p53 metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1932-6203
- Volume :
- 12
- Issue :
- 8
- Database :
- MEDLINE
- Journal :
- PloS one
- Publication Type :
- Academic Journal
- Accession number :
- 28777796
- Full Text :
- https://doi.org/10.1371/journal.pone.0181731