Abstract
Long noncoding RNAs (lncRNAs) are crucial regulatory factors in the development and progression of human malignancies. The purpose of this study was to investigate the potential mechanism of ZEB1-AS1 in pancreatic cancer (PC). The expression of ZEB1-AS1 in PC tissues and cells was assessed by RT-qPCR. The overall survival rate was evaluated using the Kaplan-Meier analysis. The association between ZEB1-AS1 and miR-505 was verified by dual-luciferase reporter assay. CCK-8 assay was employed to analyze PC cell viability. Transwell assay was employed to detect the migration and invasion of PC cells. Our results revealed that ZEB1-AS1 expression was significantly upregulated in PC tissues and cells, and the high expression of ZEB1-AS1 indicated the low overall survival rate in PC patients. Loss-of-function and gain-of-function assays indicated that knockdown of ZEB1-AS1 inhibited the cell viability, migration and invasion of PC cells, while overexpression of ZEB1-AS1 promoted PC cell progression. Moreover, ZEB1-AS1 upregulated TRIB2 expression via sponging miR-505. Finally, rescue assays demonstrated that TRIB2 overexpression partially abrogated the inhibitory effect of ZEB1-AS1 knockdown on the viability, migration and invasion of PC cells. These results confirmed that ZEB1-AS1 promoted the tumorigenesis of PC through the miR-505/TRIB2 axis, which indicated that ZEB1-AS1 might function as a biomarker for PC treatment and provide a new therapeutic direction in PC.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: Biochemical and Biophysical Research Communications
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.