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18. N-cadherin promotes thyroid tumorigenesis through modulating major signaling pathways.

Author

Da C, Wu K, Yue C, Bai P, Wang R, Wang G, Zhao M, Lv Y, and Hou P

Subjects
Antigens, CD genetics, Apoptosis, Cadherins genetics, Carcinoma, Papillary genetics, Carcinoma, Papillary pathology, Cell Cycle, Cell Line, Tumor, Cell Movement, Cell Proliferation, Cyclin-Dependent Kinase Inhibitor p16 metabolism, Epithelial-Mesenchymal Transition, Extracellular Signal-Regulated MAP Kinases metabolism, Gene Expression Regulation, Neoplastic, Humans, Neoplasm Invasiveness, Phosphatidylinositol 3-Kinase metabolism, Proto-Oncogene Proteins c-akt metabolism, RNA Interference, Retinoblastoma Protein metabolism, Thyroid Cancer, Papillary, Thyroid Neoplasms genetics, Thyroid Neoplasms pathology, Time Factors, Transfection, Antigens, CD metabolism, Cadherins metabolism, Carcinoma, Papillary metabolism, Signal Transduction, Thyroid Neoplasms metabolism
Abstract

Epithelial-mesenchymal transition (EMT), a crucial step in disease progression, plays a key role in tumor metastasis. N-cadherin, a well-known EMT marker, acts as a major oncogene in diverse cancers, whereas its functions in thyroid cancer remains largely unclear. This study was designed to explore the biological roles and related molecular mechanism of N-cadherin in thyroid tumorigenesis. Quantitative RT-PCR (qRT-PCR) and immunohistochemistry assays were used to evaluate N-cadherin expression. A series of in vitro studies such as cell proliferation, colony formation, cell cycle, apoptosis, migration and invasion assays were performed to determine the effect of N-cadherin on malignant behavior of thyroid cancer cells. Our results showed that N-cadherin was significantly upregulated in papillary thyroid cancers (PTCs) as compared with non-cancerous thyroid tissues. N-cadherin knockdown markedly inhibited cell proliferation, colony formation, cell migration and invasion, and induced cell cycle arrest and apoptosis. On the other hand, ectopic expression of N-cadherin promoted thyroid cancer cell growth and invasiveness. Mechanically, our data demonstrated that tumor-promoting role of N-cadherin in thyroid cancer was closely related to the activities of the MAPK/Erk, the phosphatidylinositol-3-kinase (PI3K)/Akt and p16/Rb signaling pathways in addition to affecting the EMT process. Altogether, our findings suggest that N-cadherin promotes thyroid tumorigenesis by modulating the activities of major signaling pathways and EMT process, and may represent a potential therapeutic target for this cancer.

Published
2017
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