Mechanism of SCD1 in promoting proliferation, migration and invasion of human papillary thyroid cancer cells

• 作者: Yue Wang Qiang Li Xin-Xin Ren Yu-Hua Sun Guo-Quan Liu
• 来源期刊: 海南医科大学学报（英文版）
• 年，卷（期）: 2021,（15）
• 所属期刊栏目: Original article
• 页码范围: 27-32
• 页数: 6页
• 语种: 英文

摘要

Objective: To investigate the effects of SCD1 on the proliferation, migration and invasion of human papillary thyroid cancer cell line TPC1. Methods: The expression of SCD1 in human thyroid follicular epithelial normal cells Nthy-ori 3-1 and thyroid papillary carcer cell lines TPC1, BCPAP and K1 was detected by Western blot. The negative control and SCD1 siRNA were transfected respectively into human thyroid papillary carcer cell line TPC1, then the expressions of SCD1 mRNA and protein in each group were tested by real-time fluorescence quantitative PCR (qRT-PCR) and Western blot. The effects of interfering SCD1 on the proliferation, migration and invasion of TPC1 cells were detected by CCK-8 method and Transwell chamber assay respectively. Meanwhile, the expression levels of epithelial-mesenchymal transition (EMT) related proteins (N-cadherin, Snail, vimentin and E-cadherin) were detected by qRT-PCR and Western blot. Results: The expression level of SCD1 in TPC1 was significantly higher than that in Nthy-ori 3-1, BCPAP and K1 (P<0.05). Compared with the blank control group (Control) and the control interference group (si-NC), the expression of SCD1 mRNA and protein in the interference SCD1 group (si-SCD1) was significantly decreased (P<0.05). The proliferation, migration and invasion of TPC1 cells were significantly inhibited after interfering with SCD1 (P <0.05). It was also found that interfering SCD1 could increase the expression of E-cadherin protein while the expression of vimentin, Snail and N-cadherin protein were inhibited significantly (P<0.05). Conclusion: Interfering SCD1 was able to inhibit the proliferation, migration and invasion of thyroid papillary cancer cell TPC1 with the potential mechanism by inhibition of the EMT procedure.