The role of Galectin-8 in Non-Small Cell Lung Cancer

• Main Authors: Sze-Fan Chen, 陳思帆
• Other Authors: Kuang-Hui Sun
• Format: Others
• Language: zh-TW
• Published: 2011
• Online Access: http://ndltd.ncl.edu.tw/handle/52079710992367274712

碩士 === 國立陽明大學 === 醫學生物技術暨檢驗學系暨研究所 === 99 === Galectins are ??galactoside-binding animal lectins defined by shared consensus amino acid sequences in the carbohydrate-recognition domain (CRD), involved in physiological processes such as adhesion, migration, cell growth, and apoptosis. Galectin-8, which has two distinct CRDs, positively or negatively regulates cell adhesion, depending on the extracellular context. Immobilized galectin-8 promotes cell adhesion and cell growth in the present of growth factors, while soluble galectin-8 induces apoptosis in the absent of growth factors. Furthermore, galectin-8 defines as a specific ligand of CD44 in rheumatoid arthritis to induce inflammatory cell apoptosis and attenuate inflammation. To investigate the relationship between galectin-8 and CD44 in lung cancer, we first examined expression of galectin-8 and CD44 in cancer cell lines using real-time PCR and flow cytometry, respectively. A549 cells expressed both CD44 and galectin-8. H1299 cells expressed higher CD44, but did not express galectin-8. Moreover, cell proliferation of H1299 cells was significantly reduced after treatment of recombinant galectin-8 in the serum-free condition, but recovered after treatment of CD44 neutralized antibody or CD44 knockdown or galectin-8 inhibitors. These results indicated that galectin-8 might regulate cell proliferation in a CD44-dependent manner. In addition, upon knockdown of galectin-8 in A549 cells, expression of CD44 was reduced; cell migration, cell invasion and colony formation were also decreased, while cell proliferation did not change. These findings suggest that galectin-8 might regulate lung cancer progression through CD44 expression.