Effect of MYEOV on Proliferation and Migration of Human Pancreatic Cancer Cells

• Main Authors: LYU Gen, YAN Jun, REN Longfei, ZHOU Wence
• Format: Article
• Language: zho
• Published: Magazine House of Cancer Research on Prevention and Treatment 2020-05-01
• Series: Zhongliu Fangzhi Yanjiu
• Subjects: pancreatic cancer; myeov; orphan gene; tgf-β pathway; proliferation; migration
• Online Access: http://html.rhhz.net/ZLFZYJ/html/8578.2020.19.1387.htm

Objective To investigate the expression of MYEOV in human pancreatic cancer cells and its effect on the proliferation and migration of pancreatic cancer SW1990 cells after knockdown. Methods The lentiviral vector GV248 was constructed and infected SW1990 cells to obtain two experimental groups (SW1990-sh1 and SW1990-sh2), while the blank plasmid was transfected as a negative control group and the untreated cells were taken as blank control group. MYEOV mRNA and protein expression were detected by qPCR and Western blot before and after transfection. The cells proliferation was determined by CCK-8 assay; the cell migration ability was analyzed by scratch test; The mRNA expression of SMADs in the TGF-β/SMAD signaling pathway was detected by qPCR. Results Compared with the pancreatic ductal epithelium cell line HPDE6, the mRNA expression of MYEOV in six pancreatic cancer cells were significantly increased (P < 0.01). However, low expression of MYEOV protein was detected only in PANC-1 and SW1990 cells. The mRNA and protein expression of MYEOV in the experimental groups were significantly downregulated. The proliferation and migration of SW1990 cells were lower than the control group (P < 0.001). MYEOV knockdown could reduce the mRNA expression of SMAD1, SMAD4, SMAD5 and SMAD9 in TGF-β pathway, while the expression of SMAD2, SMAD3 and SMAD7 mRNA were only down-regulated in the SW1990-sh2 group (P < 0.001). Conclusion MYEOV mRNA is overexpressed in pancreatic cancer cells. MYEOV could promote the proliferation and migration of pancreatic cancer cells via TGF-β/SMAD pathway.