To metastasize, tumor cells must acquire abilities to penetrate surrounding normal tissues and overcome barriers of dissemination and distant growth such as invasion, anoikis resistance, evasion of immune surveillance, extravasation, colonization, and growth in new microenvironments. Recent evidence suggests that galectin-3, a galactose binding protein, can promote metastasis by regulating detachment of cancer cells. Moreover, highly metastatic human breast cancer cells show higher levels of expression of galectin-3 and overexpression of galectin-3 enhances cell motility and invasiveness in lung cancer cells, suggesting that galectin-3 regulates cancer metastasis. However, the mechanism by which galectin-3 promotes metastasis has not been fully understood. We demonstrated here that overexpression of galectin-3 induced Epithelial-to-Mesenchymal Transition (EMT) and EMT induced by galectin-3 overexpression was remarkable in serum deprivation condition. The cell-cell adhesion molecule E-cadherin is stabilized by linking intracellularly with the actin cytoskeleton but overexpression of galectin-3 weakened the interaction of E-cadherin with cytoskeleton. Additionally, we found that galectin-3 overexpressing HT-29 cells were more resistant to anoikis stress and serum deprivation than parental HT-29 cells. Based on these findings we propose that galectin-3 is an important molecule that regulates cancer metastasis through induction of EMT and anoikis resistance.
저자
Jeong Gu Kang [ Cancer Biomarkers Development Research Center, KRIBB, Daejeon 305-806, Korea ]
Yong-Sam Kim [ Cancer Biomarkers Development Research Center, KRIBB, Daejeon 305-806, Korea ]
Jeong-Heon Ko [ Cancer Biomarkers Development Research Center, KRIBB, Daejeon 305-806, Korea ]
본 학회는 화학, 생화학, 분자생물학, 미생물학, 식품공학, 의학, 약학, 유전공학 및 생물공학, 환경 및 기타 공업 등 전 분야의 탄수화물관련 이론과 기술을 연구 발전시키고 산학협동을 통해 이를 보급하여 국내 관련 산업의 발전 및 국민생활의 과학화에 기여하고자 하며, 이러한 목표와 비젼의 실현을 위해 회원들이 적극적인 참여와 활동을 전개하고자 한다.