Gene map locus 14q21-q22
Gene function
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 revealed that hepatocellular carcinoma (HCC) frequently expressed significant levels of this lectin; 76% were immunohistochemically positive. Further investigations showed that galectin-3 expression in HCC is independent of whether the patient had prior hepatitis B virus infection (Hsu et al., 1999). Hsu et al. (1999) suggested that deregulated expression of galectin-3 can result in tumor transformation and invasiveness, or confer propensity for tumor cell survival.
In the thyroid, expression of galectin-3 protein had been described in differentiated follicular cancer, suggesting that the immunohistochemical study of galectin-3 may be a potential marker of malignancy in thyroid neoplasms. Martins et al. (2002) analyzed galectin-3 protein and mRNA expression in thyroid tissues from 87 patients with histomorphologic diagnosis of multinodular goiter (MNG), follicular adenoma, follicular carcinoma, papillary carcinoma, and 5 normal tissues.
Yoshimura et al. (2003) found increased expression of the LGALS3 gene in human nonsmall cell lung cancer, and suggested that it may play a role in the process of metastasis in this malignancy but not in small cell lung cancer. They considered that LGALS3 may be a phenotypic marker that excludes small cell lung cancer and a novel target molecule in therapy of nonsmall cell lung cancer.
Ohshima et al. (2003) found that galectin-3 mRNA and protein are expressed throughout synovial tissue in rheumatoid arthritis (RA; 180300) and that both galectin-3 and its binding protein are found at sites of joint destruction. In addition, levels of galectin-3 in serum and synovial fluid as well as levels of its binding protein in synovial fluid were significantly elevated in RA compared to osteoarthritis and healthy controls (p less than 0.001).
Henderson et al. (2006) found that galectin-3 was upregulated in established human fibrotic liver disease. In experimental hepatic fibrosis in rats, galectin-3 upregulation was associated with induction and resolution of fibrosis.
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 revealed that hepatocellular carcinoma (HCC) frequently expressed significant levels of this lectin; 76% were immunohistochemically positive. Further investigations showed that galectin-3 expression in HCC is independent of whether the patient had prior hepatitis B virus infection (Hsu et al., 1999). Hsu et al. (1999) suggested that deregulated expression of galectin-3 can result in tumor transformation and invasiveness, or confer propensity for tumor cell survival.
In the thyroid, expression of galectin-3 protein had been described in differentiated follicular cancer, suggesting that the immunohistochemical study of galectin-3 may be a potential marker of malignancy in thyroid neoplasms. Martins et al. (2002) analyzed galectin-3 protein and mRNA expression in thyroid tissues from 87 patients with histomorphologic diagnosis of multinodular goiter (MNG), follicular adenoma, follicular carcinoma, papillary carcinoma, and 5 normal tissues.
Yoshimura et al. (2003) found increased expression of the LGALS3 gene in human nonsmall cell lung cancer, and suggested that it may play a role in the process of metastasis in this malignancy but not in small cell lung cancer. They considered that LGALS3 may be a phenotypic marker that excludes small cell lung cancer and a novel target molecule in therapy of nonsmall cell lung cancer.
Ohshima et al. (2003) found that galectin-3 mRNA and protein are expressed throughout synovial tissue in rheumatoid arthritis (RA; 180300) and that both galectin-3 and its binding protein are found at sites of joint destruction. In addition, levels of galectin-3 in serum and synovial fluid as well as levels of its binding protein in synovial fluid were significantly elevated in RA compared to osteoarthritis and healthy controls (p less than 0.001).
Henderson et al. (2006) found that galectin-3 was upregulated in established human fibrotic liver disease. In experimental hepatic fibrosis in rats, galectin-3 upregulation was associated with induction and resolution of fibrosis.
GenBank: NM_002306
Protein: EAW80660.
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