Galectin-3 induced by hypoxia promotes cell migration in thyroid cancer cells
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Jiaojiao Zheng1,*, Weihui Lu1,*, Cong Wang1,*, Yang Xing2, Xiaoning Chen2 and Zhilong Ai1
1Zhongshan Hospital of Fudan University, Shanghai, People’s Republic of China
2Key Laboratory of Glycoconjugates Research, Ministry of Public Health, Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Shanghai, People’s Republic of China
*These authors have contributed equally to this work
Zhilong Ai, email: email@example.com
Keywords: galectin-3; thyroid cancer; hypoxia; migration; Src signaling pathway
Received: December 20, 2016 Accepted: August 26, 2017 Published: September 21, 2017
Background: The aim of this study is to investigate the role of Galectin-3 in human thyroid cancer migration.
Methods: The expression of Galectin-3 in surgical specimens was investigated using immunohistochemistry and western blot. A papillary thyroid cancer cell line (B-cpap) and an anaplastic thyroid cancer cell line (8305c) were transfected with short-hairpin RNA against Galectin-3 (Gal-3-shRNA). Low-molecular citrus pectin (LCP) was also used to antagonize Galectin-3. The migration and invasion of the cell lines were examined. The related signaling pathways were investigated to explore the Galectin-3 mechanism of action.
Results: Galectin-3 was highly expressed in metastasized thyroid cancers. Knocking down and antagonizing Galectin-3 significantly suppressed the migration of thyroid cancer cells. Knocking down Galectin-3 inhibited the activity of Wnt, MAPK, Src and Rho signaling pathways. Galectin-3 was up-regulated via HIF-1α in a hypoxic environment. Galectin-3 knockdown could reduce cell motility in hypoxic environments.
Conclusion: This study suggests that Galectin-3 could act as a modulator of thyroid cancer migration, especially in hypoxic microenvironments. This regulation function of Galectin-3 may work through multiple signaling pathways.
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