ABSTRACT
@# Objective: To investigate the expression of ECT2 (epithelial Transforming sequence 2) gene in human pancreatic ductal adenocarcinoma (PDAC) and its effect on the proliferation and apoptosis of pancreatic cancer cells. Methods: Carcinoma tissues and corresponding para-carcinoma tissues from 35 PDAC patients at Changhai Hospital Affiliated to Naval Medical University from July 2018 to March 2019 were collected for this study. The differentially expressed genes in pancreatic cancer were screened out by using Gene Expression Omnibus (GEO) Database. Then, the related gene expression in PDAC and its relation with patients’survival were analyzed by The Cancer Genome Atlas (TCGA) database. QPCR and immunohistochemistry were used to verify the mRNAand protein expressions of ECT2 in human PDAC samples. To explore the effect of ECT2 on the biological behaviors of pancreatic cancer cells, si-RNA was used to silence the ECT2 gene in pancreatic cancer PANC-1 cells, and CCK-8 proliferation assay and Flow cytometry were used to detect the proliferation and apoptosis rate of PANC-1 cells after ECT2 silence. Finally, the expressions of apoptosis-related proteins were detected by WB. Results: The differentially expressed gene-ECT2, was screened out by analyzing the gene expression profiles of human pancreatic cancer in GEO database. TCGA database analysis showed that ECT2 was highly expressed in pancreatic cancer tissues (t=4.005, P<0.05) and significantly correlated with patients’survival (P< 0.01). Moreover, it is also verified that ECT2 was highly expressed in PDAC tissues at mRNA (1.01±0.06 vs 4.25±0.12; t=24.09， P<0.01) and protein level. After ECT2 silence in PANC-1 cells, the proliferation rate was decreased (P<0.01), while the Tamoxifeninduced apoptosis rate was increased (P<0.01), and the expressions of apoptosis-related proteins (BAX and Bcl-2) were also affected. Conclusion: ECT2 is highly expressed in human pancreatic ductal adenocarcinoma and is related with patients’survival. ECT2 promotes the proliferation and apoptosis resistance of pancreatic cancer cells, providing the basis for exploring ECT2 as a new target for the prognostic judgment and treatment of pancreatic cancer.