Purpose: To investigate the expression and function of Galectin-3 (Gal-3) in CD133+ pulmonary adenocarcinoma.
Methods: CD133+ pulmonary adenocarcinoma cells were separated by MACS from excised pulmonary adenocarcinoma specimens of 11 patients. The percentage of CD133+ cells in different cells population was determined by flow cytometry (FCM). Expression of Gal-3 in cancer cells was detected by Fluorescence Quantitation RT-PCR (FQRT-PCR) and Western blot whereas extracellular expression was detected by ELISA. CD133+ cells were transfected with Gal-3 specific siRNA to explore the affects of Gal-3 inhibition on cancer cell growth and induction of CD8+ T cell apoptosis.
Results: Cells expressing CD133 constituted 90% of the CD133+ subpopulation after separation by MACS whereas they made up only 1.2% of the unsorted cell population. Expression of Gal-3 was 1.24 fold, 1.5 fold and 2 fold higher in CD133+ cells than in CD133– cells as detected by FQRT-PCR, Western blot and ELISA respectively (p < 0.05 for each). The supernatants of CD133+ cells induced apoptosis of CD8+ T cells to a greater degree (27.1±2.6%) compared with supernatants from CD133– cells (10.1±2.2%), and could be down-regulated by lactose, anti-galectin-3 polyclonal antibody and Gal-3 siRNA. Downregulation of Gal-3 resulted in significant inhibition of cancer cell growth in vitro.
Conclusion: Gal-3 is expressed at a relatively higher level in CD133+ lung adenocarcinoma cells and could induce CD8+ T cell apoptosis in vitro, both of which could be down-regulated by Gal-3 siRNA. These findings indicate that Gal-3 may play an important role during oncogenesis, implying a potential therapeutic target for pulmonary adenocarcinoma.
Alpha-syntrophin deficiency protects against non-alcoholic steatohepatitis associated increase of macrophages, CD8+ T-cells and galectin-3 in the liver
