Published online May 7, 2021. doi: 10.3748/wjg.v27.i17.1993
Peer-review started: December 14, 2020
First decision: February 11, 2021
Revised: February 24, 2021
Accepted: March 24, 2021
Article in press: March 24, 2021
Published online: May 7, 2021
Previous studies have suggested that long non-coding RNAs (lncRNA) TP73-AS1 is significantly upregulated in several cancers. However, the biological role and clinical significance of TP73-AS1 in pancreatic cancer (PC) remain unclear.
To investigate the role of TP73-AS1 in the growth and metastasis of PC.
The expression of lncRNA TP73-AS1, miR-128-3p, and GOLM1 in PC tissues and cells was detected by quantitative real-time polymerase chain reaction. The bioinformatics prediction software ENCORI was used to predict the putative binding sites of miR-128-3p. The regulatory roles of TP73-AS1 and miR-128-3p in cell proliferation, migration, and invasion abilities were verified by Cell Counting Kit-8, wound-healing, and transwell assays, as well as flow cytometry and Western blot analysis. The interactions among TP73-AS1, miR-128-3p, and GOLM1 were explored by bioinformatics prediction, luciferase assay, and Western blot.
The expression of TP73-AS1 and miRNA-128-3p was dysregulated in PC tissues and cells. High TP73-AS1 expression was correlated with a poor prognosis. TP73-AS1 silencing inhibited PC cell proliferation, migration, and invasion in vitro as well as suppressed tumor growth in vivo. Mechanistically, TP73-AS1 was validated to promote PC progression through GOLM1 upregulation by competitively binding to miR-128-3p.
Our results demonstrated that TP73-AS1 promotes PC progression by regulating the miR-128-3p/GOLM1 axis, which might provide a potential treatment strategy for patients with PC.
Core Tip: In this study, the expression level of TP73-AS1 in pancreatic cancer (PC) was measured and its clinical significance was assessed. In vitro and in vivo experiments were performed to determine the roles of TP73-AS1 in the progression and development of PC. Moreover, the underlying molecular mechanisms were also illustrated, which could provide a novel therapeutic target for patients with PC.