APOBEC3B and IL-6 form a positive feedback loop in hepatocellular carcinoma cells

被引：18

作者：

Li, Shuran ^{[1
]}

Bao, Xueyang ^{[1
]}

Wang, Duowei ^{[1
]}

You, Linjun ^{[1
]}

Li, Xianjing ^{[1
]}

Yang, Hongbao ^{[1
]}

Bian, Jinsong ^{[2
]}

Wang, Yun ^{[1
]}

Yang, Yong ^{[1
]}

机构：

[1] China Pharmaceut Univ, Ctr New Drug Safety Evaluat & Res, Jiangsu Key Lab Drug Discovery Metab Dis, State Key Lab Nat Med, Nanjing 211198, Jiangsu, Peoples R China

[2] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Pharmacol, Singapore 117597, Singapore

来源：

SCIENCE CHINA-LIFE SCIENCES | 2017年 / 60卷 / 06期

基金：

中国国家自然科学基金;

关键词：

APOBEC3B; interleukin-6; hepatitis; hepatocellular carcinoma; HuR; MESSENGER-RNA; TNF-ALPHA; EXPRESSION; DNA; DEAMINATION; PROGRESSION; STABILITY; PROTEINS; PATTERNS; MUTATION;

D O I：

10.1007/s11427-016-9058-6

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

APOBEC3 protein families, a DNA cytidine deaminase, were up-regulated in multiple tumors. However, the relationship between Hepatocellular carcinoma (HCC) and APOBEC3B (A3B) remains unknown. It has been confirmed that interleukin-6 (IL-6) has significant impacts on oncogenesis of HCC. Here, we reported that the expression of IL-6 was substantially up-regulated by A3B in HepG2 cells. A3B induced IL-6 expression through relocating HuR to enhance the IL-6 mRNA stability. Further analysis indicated that IL-6 also increased the expression of A3B through JAK1/STAT3 signaling pathway, which formed a positive feedback to maintain the continuous expression of A3B and IL-6, and thereby promoted the prolonged non-resolving inflammation. Collectively, these findings suggest that A3B is essential for oncogenesis of HCC, and is a potential target for preventive intervention.

引用

页码：617 / 626

页数：10