临床与实验病理学杂志2024，Vol.40Issue(12)：1287-1292,1299,7.DOI:10.13315/j.cnki.cjcep.2024.12.009
SETD7通过PI3K-AKT信号通路调节胰腺癌细胞的增殖和迁移
SETD7 regulates the proliferation and migration of pancreatic cancer cells via the PI3K/AKT signaling pathway
摘要
Abstract
Purpose This study aims to explore the role of SETD7 in the occurrence and progression of pancreatic cancer and its underlying mechanisms.Methods The expression of SETD7 in pancreatic cancer samples was studied using the Gene Expression Profiling Interactive Analysis(GEPIA)online data-base.The Kaplan-Meier Plotter database was used to analyze the impact of SETD7 expression on overall survival(OS)and re-lapse-free survival(RFS)in pancreatic cancer patients.The proliferation and migration abilities of pancreatic cancer cells were evaluated using the CCK-8 colony formation,Transwell,and scratch healing assays.Western blot was used to investigate the regulatory effects of SETD7 on the PI3K/AKT pathway.Re-sults By analyzing GEPIA database,we found that SETD7 was upregulated in pancreatic cancer(P＜0.05),the Kaplan-Meier Plotter database analysis showed that OS and DFS were both sig-nificantly higher in the low SETD7 expression group than those in the high SETD7 expression(P＜0.001).We found that the ex-pression of SETD7 in PC was higher compared with their adjacent non-tumorous tissues(P＜0.01).Upregulation of SETD7 pro-moted the proliferation and migration of pancreatic cancer cells(P＜0.01 or P＜0.05),while downregulation of SETD7 led to decreased proliferation and migration abilities(P＜0.01 or P＜0.05).We also found that SETD7 knockdown-induced reduction of p-PI3K and p-AKT.Overexpression of SETD7 resulted in in-creased expression of p-PI3K and p-AKT.Additionally,SETD7-KD significantly upregulated the expression of the epithelial marker E-cadherin and inhibited the expression of the mesenchy-mal marker,N-cadherin and vimentin.When SETD7 was in-creased,the expression levels of E-cadherin were decreased,and the protein expression levels of N-cadherin and vimentin were in-creased.SETD7 could regulate the PI3K/AKT signaling pathway and promote the epithelial-mesenchymal transition(EMT)of pancreatic cancer cells.Conclusion SETD7 promotes the pro-liferation and migration of pancreatic cancer cells and regulates EMT by activating the PI3K/AKT signaling pathway.SETD7 may serve as a potential therapeutic target for pancreatic cancer.关键词
胰腺癌/SETD7/PI3K/AKT/增殖/迁移Key words
pancreatic cancer/SETD7/PI3K/AKT/prolifera-tion/migration分类
医药卫生引用本文复制引用
高丝,李青,高丽丽..SETD7通过PI3K-AKT信号通路调节胰腺癌细胞的增殖和迁移[J].临床与实验病理学杂志,2024,40(12):1287-1292,1299,7.基金项目
浦东新区科技发展基金(PKJ2020-Y40)、上海市卫健委卫生行业临床研究专项项目(202140099) （PKJ2020-Y40）
