CD133+ human pulmonary adenocarcinoma cells induce apoptosis of CD8+T cells by highly expressed galectin-3

Wan Li; Wang Jian-jun; Zhou Xue-Feng; Zhao Feng
February 2010
Clinical & Investigative Medicine;Feb2010, Vol. 33 Issue 1, pE44
Academic Journal
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 (FQRTPCR) 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.


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