Abstract |
Epirubicin, which is a conventional chemotherapeutic drug for gastric cancer, has innate and adaptive chemoresistance. Recent studies revealed that epirubicin could induce autophagy as a defensive mechanism in drug resistance of mammary carcinoma. Another study implied that DJ-1 may be a chemoresistance-related gene. But the association between DJ-1 and drug resistance of epirubicin in gastric cancer is still ambiguous. In the present report, we explored whether and how DJ-1 conduced to epirubicin-induced apoptosis in gastric cancer. Epirubicin dose-dependently increased the expression of DJ-1 and induced autophagy. Knockdown of DJ-1 notably enhanced epirubicin-induced cell apoptosis, whereas overexpression of DJ-1 attenuated epirubicin-induced cell apoptosis. Further studies revealed that down-regulation of DJ-1 modulated epirubicinactivated autophagy which augmented epirubicin-induced apoptosis. In conclusion, our results validated that DJ-1 reduced epirubicin-induced apoptosis in gastric cancer cells via modulating epirubicin-activated autophagy.
|
Authors | Xue-Kai Pan, Fei Su, Li-Hua Xu, Zhang-Shuo Yang, Dan-Wen Wang, Li-Jie Yang, Fan-Zheng Kong, Wei Xie, Mao-Hui Feng |
Journal | Current medical science
(Curr Med Sci)
Vol. 38
Issue 6
Pg. 1018-1024
(Dec 2018)
ISSN: 2523-899X [Electronic] China |
PMID | 30536064
(Publication Type: Journal Article)
|
Chemical References |
- Epirubicin
- PARK7 protein, human
- Protein Deglycase DJ-1
|
Topics |
- Apoptosis
(drug effects)
- Autophagy
(drug effects)
- Cell Line, Tumor
- Drug Resistance, Neoplasm
(drug effects)
- Epirubicin
(pharmacology)
- Humans
- Protein Deglycase DJ-1
(metabolism)
- Stomach Neoplasms
(drug therapy, metabolism, pathology)
|