Metformin inhibits the senescence and senescence-associated secretory phenotype of gastric cancer BGC823 cells induced by doxorubicin
DOI：10.3872/j.issn.1007-385x.2020.08.006
- VernacularTitle:二甲双胍抑制多柔比星诱导的胃癌BGC823细胞衰老及其相关分泌表型
- Author:
HUANG Hejing
1
;
ZHANG Xin
2
;
ZHU Zhenxin
2
;
WEI Ziran
2
;
YANG Dejun
2
;
CAI Qingping
2
Author Information
1. a. Department of Ultrasound
2. b. Department of Gastrointestinal Surgery, Changzheng Hospital, Naval Military Medical University, Shanghai 200003, China
- Publication Type:Journal Article
- Keywords:
gastric cancer;
cell senescence;
senescence-associated secretory phenotype;
metformin;
oxidative stress
- From:
Chinese Journal of Cancer Biotherapy
2020;27(8):874-878
- CountryChina
- Language:Chinese
-
Abstract:
[Abstract] Objective: To investigate the effect of metformin on the senescence-associated secretory phenotype (SASP) of doxorubicin-induced gastric cancer BGC823 cells. Methods: Human gastric cancer BGC823 cells were cultured in vitro and treated with doxorubicin at gradient concentrations (50, 100, 150 and 200 nmol/L). Cell senescence was detected by SA-β-gal staining, and SASP factor expression was detected by ELISA. The effects of metformin on cell senescence and SASP factor secretion induced by doxorubicin (100 nmol/L) were observed by adding gradient concentrations of metformin (0, 5, 10 and 20 mmol/L). Results: With the increase of doxorubicin concentration and treatment time, the senescence rate of gastric cancer BGC823 cells increased first and then decreased. At 96 h after 100 nmol/L doxorubicin treatment, the peak aging rate reached 68.7%, accompanied with significantly increased expressions of SASP factors IL-1a, IL-6, IL-8 and CXCL1. The proportion of senescent cells was (55.2±1.9)%, (48.7±2.2)% and (40.8±2.3)% respectively under the effects of 5, 10 and 20 mmol/L metformin, which was significantly lower than that in the non-metformin treatment group (P< 0.01). At the same time, with the increase of metformin concentration, the production of SASP factors IL-1α, IL-6, IL-8 and CXCL1 showed a gradient decline. Compared with the non-metformin treatment group, IL-6 and IL-8 decreased significantly under the effect of metformin above 10 mmol/L (P<0.05 or P<0.01), while IL-1α and CXCL1 decreased significantly under the effect of 20 mmol/L metformin (all P<0.05). Conclusion: Metformin can inhibit the senescence and SASP production of gastric cancer cells induced by doxorubicin.
- Full text:20200806.pdf
