title: 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.
authors.affiliation: Division of Allergy, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA.
authors.forename: D K
authors.initials: DK
authors.lastname: Hsu
authors.forename: C A
authors.initials: CA
authors.lastname: Dowling
authors.forename: K C
authors.initials: KC
authors.lastname: Jeng
authors.forename: J T
authors.initials: JT
authors.lastname: Chen
authors.forename: R Y
authors.initials: RY
authors.lastname: Yang
authors.forename: F T
authors.initials: FT
authors.lastname: Liu
mesh_terms: D000818:Animals; D000943:Antigens, Differentiation / Q000032:analysis / Q000235:genetics*; D001706:Biopsy; D006528:Carcinoma, Hepatocellular / Q000235:genetics* / Q000473:pathology; D037502:Galectin 3; D005786:Gene Expression Regulation; D015972:Gene Expression Regulation, Neoplastic; D006509:Hepatitis B / Q000150:complications / Q000473:pathology; D006511:Hepatitis B Antigens / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D037102:Lectins / Q000032:analysis / Q000235:genetics; D008099:Liver / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D008103:Liver Cirrhosis / Q000235:genetics* / Q000473:pathology; D008113:Liver Neoplasms / Q000235:genetics* / Q000473:pathology; D051379:Mice; D009928:Organ Specificity; D011401:Promoter Regions, Genetic; D013154:Spleen / Q000378:metabolism; D013950:Thymus Gland / Q000378:metabolism; D015534:Trans-Activators / Q000235:genetics / Q000378:metabolism; D015533:Transcriptional Activation; D014407:Tumor Cells, Cultured; D054334:Viral Regulatory and Accessory Proteins
chemical_list: D000943:Antigens, Differentiation; D037502:Galectin 3; D006511:Hepatitis B Antigens; D037102:Lectins; D015534:Trans-Activators; D054334:Viral Regulatory and Accessory Proteins; C057628:hepatitis B virus X protein