DPP4 gene silencing inhibits proliferation and epithelial-mesenchymal transition of papillary thyroid carcinoma cells through suppression of the MAPK pathway.
作者： X. Hu , S. Chen , C. Xie , Z. Li , Z. Wu
DOI: 10.1007/S40618-020-01455-7
关键词:
摘要: Papillary thyroid carcinoma (PTC) is characterized by epithelial malignancy and the most prevalent neoplasm with best overall prognosis. Notably, recently published studies have indicated remarkably high expression of dipeptidyl peptidase 4 (DPP4) in PTC. However, underlying molecular mechanism regulatory factors PTC progression remain unknown. Therefore, current study aimed to elucidate effects DPP4 gene silencing on further investigated whether related mitogen-activated protein kinase (MAPK) pathway. Herein, microarray-based profiling was conducted identify differentially expressed genes between tumor tissue normal as well signaling pathway involved pathogenesis. Moreover, quantification performed assess tissues collected from 65 patients. In addition, silenced cell lines (GLAG-66 TPC-1) through siRNA-mediated knockdown or sitagliptin (inhibitor DPP4)-mediated inhibition MAPK cellular processes, including proliferation, apoptosis, epithelial-to-mesenchymal transition (EMT). Intriguingly, our data revealed markedly tissues. GLAG-66 TPC-1 cells, resulted significantly reduced ERK1/2, JNK1, P38 MAPK, VEGF, FGFR-1, TGF-β1, Snail, HIF-1α, N-cadherin, Bcl-2 along with phosphorylation whereas E-cadherin Bax increased. Furthermore, found hinder proliferation potentiate apoptosis. Collectively, present demonstrated that inhibits EMT promotes apoptosis via suppression pathway, thus highlighting a possible progression.
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