CARD10 promotes apoptosis inhibition of hepatocellular carcinoma cells by activating NF-κB pathway
10.3872/j.issn.1007-385x.2020.03.012
- VernacularTitle:CARD10通过活化NF-κB信号进而促进肝癌细胞凋亡抵抗
- Author:
JIA Kaiwei
1
,
2
;
ZHOU Ye
1
,
2
;
LI Zhenyang
1
,
2
;
ZHANG Liyuan
1
,
2
;
HOU Jin
1
,
2
Author Information
1. (National Key Laboratory of Medical Immunology &
2. Institute of Immunology, Naval Military Medical University
- Publication Type:Journal Article
- Keywords:
hepatocellular carcinoma (HCC);
caspase recruitment domain family member 10 (CARD10);
apoptosis;
NF-κB
- From:
Chinese Journal of Cancer Biotherapy
2020;27(3):289-294
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the expression of CARD10 in hepatocellular carcinoma (HCC) tissues, and the roles of CARD10 in HCC progression especially apoptosis inhibition. Methods: The expression of CARD10 was examined in pared non-tumor liver tissues and HCC tissues using qRT-PCR, and their correlation with HCC TNM stage was analyzed using Spearman’s rank correlation assay in SPSS 17.0. In HCC cells with CARD10 overexpression or knockdown, cytometry using Annexin-V/PI labeling was used to measure apoptosis, and Western blotting was used to determine the activation of NF-κB pathway. Results: CARD10 expression was significantly increased in HCC tissues as compared to that in pared non-tumor liver tissues (P<0.01), and the increased CARD10 in HCC was positively correlated with TNM staging (P<0.01). The apoptosis of HCC cell lines SMMC-7721 and BEL-7402 was inhibited by CARD10 overexpression while promoted by CARD10 knockdown, and the pro-survival NF-κB pathway was also enhanced by CARD 10 over-expression while suppressed by CARD10 knockdown. Conclusion: CARD10 expression is increased in HCC tissues and positively correlated with HCC progression. CARD10 inhibits HCC apoptosis by promoting the activation of NF-κB pathway. [Key words] hepatocellular carcinoma (HCC); caspase recruitment domain family member 10 (CARD10); apoptosis; NF-κB
- Full text:20200312.pdf
