title: Increased glyceraldehyde-3-phosphate dehydrogenase expression indicates higher survival rates in male patients with hepatitis B virus-accociated hepatocellular carcinoma and cirrhosis.
abstract: Elevated expression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) has been reported in different human malignancies. To understand its role in hepatitis B virus (HBV) infection-associated hepatocellular carcinoma (HCC), the expression of GAPDH was quantitatively measured in a cohort of 72 male HCC patients without preoperative treatment, all with evidence of chronic HBV infection. Using C-terminal banding protein 1 (CTBP1) or hypoxanthine phosphori-bosyltransferase 1 (HPRT1) as reference genes, the level of GAPDH mRNA in tumor tissue was found to be significantly higher compared with that in paired non tumor tissues (P=0.0087 for CTBP1; P=0.0116 for HPRT1). Accordingly, compared with the non-tumor tissue, 37.5% (27/72) of patients' tumor tissues had a more than 2-fold increase of GAPDH expression. Furthermore, following knockdown GAPDH expression via siRNA transient transfection, HepG2 cells exhibited enhanced resistance to cytosine arabinoside (IC50, 308.28 µM vs. 67.68 µM in the control; P=0.01). Notably, higher GAPDH expression was significantly associated with lower liver fibrosis score (P=0.0394) and a tendency towards higher survival rates for patients with HCC. To the best of our knowledge, the present study is the first study to report that the elevated expression levels of GAPDH in HCC tumor tissue may be relevant to an improved fibrosis score and survival probability in male patients with HBV infection; however, the underlying mechanism requires further investigation.
authors.affiliation: Beijing Artificial Liver Treatment and Training Center, Beijing Youan Hospital, Capital Medical University, Beijing 100069, P.R. China.
authors.forename: Shuang
authors.initials: S
authors.lastname: Liu
authors.affiliation: Beijing Artificial Liver Treatment and Training Center, Beijing Youan Hospital, Capital Medical University, Beijing 100069, P.R. China.
authors.forename: Pengfei
authors.initials: P
authors.lastname: Zhu
authors.affiliation: Department of Hepatobiliary Surgery, Henan Cancer Hospital, Zhengzhou, Henan 450008, P.R. China.
authors.forename: Ling
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Beijing Artificial Liver Treatment and Training Center, Beijing Youan Hospital, Capital Medical University, Beijing 100069, P.R. China.
authors.forename: Zhuo
authors.initials: Z
authors.lastname: Li
authors.affiliation: Department of Nutrition and Food Hygiene, College of Public Health, Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
authors.forename: Quanjun
authors.initials: Q
authors.lastname: Lv
authors.affiliation: Beijing Artificial Liver Treatment and Training Center, Beijing Youan Hospital, Capital Medical University, Beijing 100069, P.R. China.
authors.forename: Sujun
authors.initials: S
authors.lastname: Zheng
authors.affiliation: Beijing Artificial Liver Treatment and Training Center, Beijing Youan Hospital, Capital Medical University, Beijing 100069, P.R. China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Microbiology and Infectious Disease Center, Peking University Health Science Center, Beijing 100086, P.R. China.
authors.forename: Fengmin
authors.initials: F
authors.lastname: Lu
keywords: chemotherapy; glyceraldehyde-3-phosphate dehydrogenase; hepatitis B virus; hepatocellular carcinoma; liver cirrhosis