Synergistic interaction between galectin-3 and carcinoembryonic antigen promotes colorectal cancer metastasis
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Keng-Liang Wu1,2,3, Eng-Yen Huang4,5, Wen-Ling Yeh1, Chang-Chun Hsiao2,6 and Chung-Mou Kuo1,3
1Division of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan
2Graduate Institute of Clinical Medical Sciences, Chang Gung University, Kaohsiung, Taiwan
3Chang Gung University, College of Medicine, Kaohsiung, Taiwan
4Department of Radiation Oncology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan
5School of Traditional Chinese Medicine, Chang Gung University College of Medicine, Kaohsiung, Taiwan
6Center for Shockwave Medicine and Tissue Engineering, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan
Chang-Chun Hsiao, email: email@example.com
Keywords: colorectal cancer, galectin-3, carcinoembryonic antigen, cancer cell migration
Received: February 09, 2017 Accepted: May 22, 2017 Published: June 27, 2017
In this study, we investigated the role of galectin-3 and carcinoembryonic antigen (CEA) in metastasis and survival of colorectal cancer (CRC) patients. CEA interacted with galectin-3 at the cell surface and cytoplasm of Caco2 and DLD1 CRC cells. Knocking down galectin-3 did not affect CEA expression in CRC cells. However, there was a dose-dependent increase in CRC cell migration upon addition of small amounts of exogenous CEA (≤1ng/ml). Galectin-3 knockdown blocked induction of CRC cell migration by CEA, suggesting interaction between galectin-3 and CEA was necessary for CRC cell migration. Exogenous CEA and galectin-3 synergistically promoted migration of galectin-3 knockdown DLD1 cells. Immunohistochemical analysis showed that CEA co-localized with galectin-3 in CRC patient tissues. In additon, advanced stage CRC patients had higher serum galectin-3 and CEA levels than early stage CRC patients. High serum CEA and galectin-3 levels correlated with advanced N stage and poor survival in CRC patients. These findings suggest interaction between galectin-3 and CEA promotes CRC migration and metastasis, and correlates with poor survival of CRC patients. Thus combinatorial therapy targeting galectin-3 and CEA may improve outcomes for advanced stage CRC patients.
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