Galectin-3 expression is induced in cirrhotic liver and hepatocellular carcinoma.

ABSTRACT

Galectins are a family of beta-galactoside-binding animal lectins. In particular, a widely studied member galectin-3, previously designated as epsilonBP, CBP35, Mac-2, L-29 and L-34, has been associated with assorted processes such as cell growth, tumor transformation and metastasis. Galectin-3 is expressed in various tissues and organs but is significantly absent in normal hepatocytes. However, evaluation of patient liver biopsies for galectin-3 expression resulted in the finding that hepatocellular carcinoma (HCC) frequently expressed significant levels of this lectin (76% immunohistochemically positive). Further investigation revealed that galectin-3 expression in HCC is independent of whether the patient had prior hepatitis B virus infection 14 of 18 HCC cases from HBV- patients, and 5 of 7 cases from HBV patients demonstrated positive galectin-3 immunohistochemistry. However, co-transfection studies using a galectin-3 promoter construct and an HBV-X protein (HBV-X) expression vector demonstrated that galectin-3 expression can occur through transactivation of the lectin promoter by HBV-X. Based on presently known properties of this lectin, it is possible that deregulated expression of galectin-3 can result in tumor transformation and invasiveness, or confer propensity for tumor cell survival. In addition, galectin-3 was abundantly expressed in cirrhotic liver in peripheral distribution within regenerating nodules. Such galectin-3 expression in rapidly proliferating hepatocytes in cirrhotic liver may be a result of the high mitotic index. Alternatively, it is possible that proliferating cells expressing galectin-3 are in the process of being transformed, thus indicating an early neoplastic event.