Effects of PTS on gastric cancer cells by regulating Wnt/β-catenin pathway
10.3969/j.issn.1673-9701.2024.19.006
- VernacularTitle:PTS通过调控Wnt/β-catenin通路对胃癌细胞的影响
- Author:
Jinpeng YANG
1
;
Wenhua WANG
;
Yongbo ZHANG
;
Yuying ZHANG
Author Information
1. 山东第二医科大学临床医学院,山东潍坊 261042
- Keywords:
6-pyruvoyl-tetrahydropterin synthase;
Gastric cancer;
Wnt/β-catenin signaling pathway;
Malignant biological behavior
- From:
China Modern Doctor
2024;62(19):26-32
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of 6-pyruvoyl-tetrahydropterin synthase(PTS)on gastric cancer cells.Methods The expression of PTS protein and mRNA in gastric mucosal epithelial cells GES-1 and gastric cancer cell lines HGC-27 cells,MGC-803 cells,AGS cells and MKN-45 cells were determined by Western blot(WB)and reverse transcription quantitative polymerase chain reaction(RT-qPCR).AGS cells were selected for follow-up experiments.AGS cells were divided into control(NC)group,sh-PTS group,and sh-PTS+BML-284 group.Cell proliferation was measured by CCK-8.Cell migration ability was measured by scratch healing.Cell invasion and migration were measured by Transwell assay.Apoptosis was measured by flow cytometry.The protein and mRNA levels of β-catenin,c-myc,GSK-3β and Wnt5a were detected by WB and RT-qPCR.Results The expression of PTS in gastric mucosal epithelial cells GES-1 was lower than that in gastric cancer cells,and the expression of PTS was the highest in AGS cells.Knocking down PTS could inhibit proliferation,migration and invasion of gastric cancer cells,promote cell apoptosis,decreased β-catenin,c-myc,Wnt5a protein levels,and increased GSK-3β protein levels(P＜0.05).Compared with sh-PTS group,cell proliferation,migration and invasion ability of sh-PTS+BML-284 group were enhanced,apoptosis level was decreased,protein expression of β-catenin,c-myc and Wnt5a was increased,and protein expression of GSK-3β was decreased(P＜0.05).Conclusion PTS can affect proliferation,migration,invasion and apoptosis of gastric cancer cells by mediating Wnt/β-catenin pathway.
