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

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...

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Bibliographic Details
Published inScience China. Life sciences Vol. 60; no. 6; pp. 617 - 626
Main Authors Li, Shuran, Bao, Xueyang, Wang, Duowei, You, Linjun, Li, Xianjing, Yang, Hongbao, Bian, Jinsong, Wang, Yun, Yang, Yong
Format Journal Article
LanguageEnglish
Published Beijing Science China Press 01.06.2017
Springer Nature B.V
Subjects
Animals
Biomedical and Life Sciences
Carcinoma, Hepatocellular - metabolism
Carcinoma, Hepatocellular - pathology
Cytidine deaminase
Cytidine Deaminase - metabolism
Deoxyribonucleic acid
DNA
Feedback
Hep G2 Cells
Hepatocellular carcinoma
Humans
HuR protein
IL-6
Interleukin 6
Interleukin-6 - metabolism
Janus kinase
Life Sciences
Liver cancer
Liver Neoplasms - metabolism
Liver Neoplasms - pathology
Mice, Inbred C57BL
Minor Histocompatibility Antigens - metabolism
mRNA
mRNA stability
Protein families
Research Paper
Signal transduction
Stat3 protein
Tumorigenesis
Tumors
信号通路
反馈回路
白细胞介素-6
肝细胞癌
胞嘧啶脱氨酶
HuR
hepatitis
interleukin-6
hepatocellular carcinoma
APOBEC3B
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Summary: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 A3 B in HepG2 cells. A3 B 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 A3 B through JAK1/STAT3 signaling pathway, which formed a positive feedback to maintain the continuous expression of A3 B and IL-6, and thereby promoted the prolonged non-resolving inflammation. Collectively, these findings suggest that A3 B is essential for oncogenesis of HCC, and is a potential target for preventive intervention.
Bibliography:APOBEC3B interleukin-6 hepatitis hepatocellular carcinoma HuR
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 A3 B in HepG2 cells. A3 B 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 A3 B through JAK1/STAT3 signaling pathway, which formed a positive feedback to maintain the continuous expression of A3 B and IL-6, and thereby promoted the prolonged non-resolving inflammation. Collectively, these findings suggest that A3 B is essential for oncogenesis of HCC, and is a potential target for preventive intervention.
11-5841/Q
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ISSN:1674-7305
1869-1889
1869-1889
DOI:10.1007/s11427-016-9058-6