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The promoting effect of adiponectin in hepatocellular carcinoma
Author(s) -
Chen MingJenn,
Yeh YaoTsung,
Lee KingTeh,
Tsai ChiaJung,
Lee HaoHsien,
Wang ShenNien
Publication year - 2012
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.23059
Subject(s) - adiponectin , medicine , adipokine , hepatocellular carcinoma , endocrinology , radioimmunoassay , insulin resistance , albumin , alkaline phosphatase , carcinoma , obesity , biology , biochemistry , enzyme
Background and Objectives Adipokines may explain the newly established association of obesity with hepatocellular carcinoma (HCC). This study investigated if adiponectin levels in HCC patients differed from healthy controls and their potential effect in the development of HCC. Methods Radioimmunoassay was used to determine serum adiponectin levels of 65 HCC patients and 165 healthy controls. The expressions of adiponectin protein in the tumor and adjacent non‐tumor parts were examined by the immunoblotting method. Cell proliferation assays were used to assess the bioeffects of adiponectin in two human liver cancer cell lines. Results Serum adiponectin levels were significantly higher in the HCC patients than the controls. Significant correlations of serum adiponectin levels with serum triglyceride levels and insulin resistance were found in the controls, but not in the HCC patients. In contrast, serum adiponectin levels significantly correlated with serum albumin and alkaline phosphatase levels in the HCC patients, but this trend was not observed in the controls. The expression pattern of adiponectin protein between the paired tumor and adjacent non‐tumor tissues significantly correlated with tumor size. In vitro, adiponectin increased cell proliferation in a dose‐dependent manner. Conclusions Increased adiponectin expressions were found in HCC and this increase might contribute to tumor growth. J. Surg. Oncol. 2012; 106:181–187. © 2012 Wiley Periodicals, Inc.