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
Pancreatic cancer (PC) is the fourth most frequent cause of cancer-related deaths in the world. Emerging evidence has revealed that long non-coding RNAs (lncRNAs) could play crucial roles in the progression of PC. However, the biological role and clinical significance of TP73-AS1 in PC remain unclear.
Treatments for PC are still limited, and surgical resection could be the only chance to obtain curative treatment. We hope to provide a novel therapeutic target for patients with PC.
The present study aimed to investigate the role of TP73-AS1 in the growth and metastasis of PC.
Quantitative reverse transcription-polymerase chain reaction was used to detect the expression of lncRNA TP73-AS1, miR-128-3p, and GOLM1 in PC tissues and cells. The regulatory roles of TP73-AS1 in cell proliferation, migration, and invasion ability were verified by Cell Counting Kit-8, wound-healing, and transwell assays. The bioinformatics prediction software ENCORI was used to predict the putative binding sites of miR-128-3p. The interactions among TP73-AS1, miR-128-3p, and GOLM1 were explored by bioinformatics prediction, luciferase assay, and Western blot.
Our data suggested that TP73-AS1 and miRNA-128-3p were dysregulated in PC tissues and cells. TP73-AS1 silencing inhibited PC cell proliferation, migration, and invasion in vitro as well as suppressed tumor growth in vivo. Moreover, TP73-AS1 could promote tumor growth and invasion by acting as a competing endogenous RNA to promote GOLM1 expression by sponging miR-128-3p in PC.
TP73-AS1 could promote PC cell proliferation and metastasis by modulating the miR-128-3p/GOLM1 axis.
TP73-AS1 could promote PC progression, which might provide a potential treatment strategy for patients with PC.