Journal
ONCOTARGET
Volume 8, Issue 35, Pages 58601-58610Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.17380
Keywords
hepatic steatosis; chronic hepatitis B; hepatocellular carcinoma cells
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Funding
- Capital Science and Technology Development Fund [2014-1-2181]
- Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding [ZYLX201610]
- Beijing Municipal Administration of Hospitals'Ascent Plan [DFL20151602]
- National Science Fund [81672725, 81401970]
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Aim: To characterize the effect of hepatic steatosis (HS) on the progression of chronic hepatitis B. Methods: A total of 162 chronic hepatitis B (CHB) patients confirmed by liver biopsy were involved in this study. All subjects were prospectively followed-up for 5 years in real-life clinical practice. Fibrosis stage was determined using aspartate aminotransferase-to-platelet ratio index (APRI). The end-point was cirrhosis, liver cancer or death. The effects of steatosis on the biological behavior of hepatocellular carcinoma cells were investigated using oleic acid-induced lipid accumulation in HepG(2), HLE, PLC, and SMMC-7721 cells. Results: Mean age, body mass index, and serum cholesterol were significantly higher in CHB patients with HS than those without HS at baseline (p< 0.05). The APRI was lower in patients without HS at baseline (p< 0.05). Compared to patients with HS, APRI of patients without HS decreased significantly during the follow-up period (p<0.05). The 5-year cumulative incidence of cirrhosis were 4.17% and 5.19% in patients without and with HS, respectively (p>0.05). The multivariate analysis showed that older (RR 1.07, 95% CI 0.996-1.149, p = 0.065) and S3 stage of liver fibrosis (RR 3.50, 95% CI 0.812-15.117, p=0.093) were risk factors for the progression to cirrhosis. In vitro, cell steatosis promoted proliferation and migration of HCC cells and conferred cell cycle at S phase. Conclusion: The older and S3 stage of fibrosis may be risk factors for progression to cirrhosis in CHB patients with HS. HS may aggravate liver disease, promoting HCC progression.
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