Relationship of PPARG, PPARGC1A, and PPARGC1B polymorphisms with susceptibility to hepatocellular carcinoma in an eastern Chinese Han population
Authors Zhang S, Jiang J, Chen Z, Wang Y, Tang W, Chen Y, Liu L
Received 15 March 2018
Accepted for publication 23 May 2018
Published 8 August 2018 Volume 2018:11 Pages 4651—4660
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Sanjeev Srivastava
Sheng Zhang,1,* Jiakai Jiang,1,* Zhan Chen,2 Yafeng Wang,3 Weifeng Tang,4 Yu Chen,5–7 Longgen Liu8
1Department of General Surgery, Changzhou Third People’s Hospital, Changzhou, Jiangsu Province, China; 2Department of Thoracic Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian Province, China; 3Department of Cardiology, People’s Hospital of Xishuangbanna Dai Autonomous Prefecture, Jinghong, Yunnan Province, China; 4Department of Cardiothoracic Surgery, Affiliated People’s Hospital of Jiangsu University, Zhenjiang, Jiangsu Province, China; 5Cancer Bio-immunotherapy Center, Fujian Cancer Hospital and Fujian Medical University Cancer Hospital, Fuzhou, Fujian Province, China; 6Department of Medical Oncology, Fujian Cancer Hospital and Fujian Medical University Cancer Hospital, Fuzhou, Fujian Province, China; 7Fujian Provincial Key Laboratory of Translational Cancer Medicine, Fuzhou, Fujian Province, China; 8Department of Liver Disease, Changzhou Third People’s Hospital, Changzhou, Jiangsu Province, China
*These authors contributed equally to this work
Background: PPARG, PPARGC1A, and PPARGC1B polymorphisms may be implicated in the development of cancer.
Participants and methods: In this study, we selected PPARG rs1801282 C>G and rs3856806 C>T, PPARGC1A rs2970847 C>T, and PPARGC1B rs7732671 G>C and rs17572019 G>A single-nucleotide polymorphisms to explore the relationship between these polymorphisms and hepatocellular carcinoma (HCC) risk. A total of 584 HCC patients and 923 controls were enrolled.
Results: We found that PPARG rs1801282 C>G polymorphism was correlated with a decreased susceptibility of HCC (CG vs CC, adjusted OR 0.47, 95% CI 0.27–0.82, P=0.007; CG/GG vs CC, adjusted OR 0.52, 95% CI 0.31–0.88, P=0.015). However, PPARG rs3856806 C>T polymorphism was a risk factor for HCC (TT vs CC, adjusted OR 2.33, 95% CI 1.25–4.36, P=0.008; TT vs CT/CC, adjusted OR 2.26, 95% CI 1.22–4.17, P=0.010). In a subgroup analysis by chronic hepatitis B virus (HBV)-infection status, age, sex, alcohol use, and smoking status, a significant association between PPARG rs1801282 C>G polymorphism and a decreased risk of HCC in male, ≥53 years, never-smoking, never-drinking, and nonchronic HBV-infection-status subgroups was found. However, we found PPARG rs3856806 C>T polymorphism increased the risk of HCC in never-smoking, never-drinking, and nonchronic HBV-infection-status subgroups. Haplotype-comparison analysis indicated that Crs1801282Trs3856806Crs2970847Grs7732671Grs17572019, Crs1801282Trs3856806Trs2970847Grs7732671Grs17572019, and Crs1801282Crs3856806Crs2970847Crs7732671Ars17572019 haplotypes increased the risk of HCC. PPARG Crs1801282Trs3856806 and Grs1801282Crs3856806 haplotypes also influenced the risk of HCC.
Conclusion: In conclusion, our findings suggest PPARG polymorphisms may influence the susceptibility of HCC. The PPARG, PPARGC1A, and PPARGC1B haplotypes might be associated with HCC risk.
Keywords: PPARG, PPARGC1A, PPARGC1B, polymorphism, risk, hepatitis B virus, hepatocellular carcinoma
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