4.7 Article

Galectin-3 is associated with a poor prognosis in primary hepatocellular carcinoma

Journal

JOURNAL OF TRANSLATIONAL MEDICINE
Volume 12, Issue -, Pages -

Publisher

BMC
DOI: 10.1186/s12967-014-0273-3

Keywords

Galectin-3; Hepatocellular carcinoma; Angiogenesis; Apoptosis; Prognostic factor

Funding

  1. National Natural Science Foundation of China [30973398]
  2. Guangdong Natural Science Foundation [925100890]
  3. Natural Science Foundation of Guangdong Province, China [2011A030400004]

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Background: Galectin-3, a member of the beta-galactoside-binding lectin family, is a multifunctional protein with various biological functions, including the proliferation and differentiation of tumor cells, angiogenesis, cancer progression, and metastasis. We aimed to clarify if expression of galectin-3 is related to the clinicopathological characteristics and prognosis of hepatocellular carcinoma (HCC) patients, and to explore the possible mechanisms of galectin-3 in hepatocellular carcinoma. Methods: First, we investigated galectin-3 mRNA and protein expression by using RT-PCR and Western blotting. Second, tissues from 165 HCC patients were used to evaluate clinicopathological characteristics and prognosis through immunohistochemical analyses. Furthermore, the functions of galectin-3 were analyzed with respect to the proliferation, cell cycle, apoptosis, migration, and invasion of HCC cell lines. Finally, we analyzed galectin-3 expression and micro-vessel density (MVD) by immunohistochemistry (IHC) to find its correlation with angiogenesis in Hepatocellular Carcinoma. Flow cytometer was used to explore apoptosis and Western-blot was used to detect the pathway proteins of apoptosis. Results: Galectin-3 showed high expression at the mRNA and protein levels in HCC cancer tissues and cell lines. Clinicopathological analyses revealed that increased expression of galectin-3 in tumors was closely associated with a poor prognosis. Galectin-3 knockdown by siRNA significantly inhibited cell growth, migration, and invasion, and induced apoptosis in HCC cells in vitro, whereas galectin-3 overexpression promoted cell growth, migration, and invasion. Correlation analysis of galectin-3 expression and micro-vessel density (MVD) showed that galectin-3 expression in tumor cells stimulates angiogenesis. The observed regulation of cell apoptosis was accompanied by the galectin-3-mediated modulation of caspase3 signaling pathways in HCC cells. Conclusions: These data suggest that galectin-3 plays an important part in HCC progression and may serve as a prognostic factor for HCC.

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