Published online Nov 15, 2022. doi: 10.4251/wjgo.v14.i11.2183
Peer-review started: August 21, 2022
First decision: September 13, 2022
Revised: September 28, 2022
Accepted: October 27, 2022
Article in press: October 27, 2022
Published online: November 15, 2022
Processing time: 85 Days and 19.2 Hours
TRIM55 plays important role in hepatocellular carcinoma and lung adenocarcinoma. However, little is known about the role of TRIM55 in gastric cancer (GC).
To discover the targets for the diagnosis, treatment and prognosis prediction of GC.
To explore the biological function of TRIM55 and its underlying molecular mechanism in GC.
The expression of TRIM55 was determined by quantitative real-time polymerase chain reaction and Western blot. Cell counting kit-8 assay, colony formation, wound healing assay and transwell assay were used to investigate the TRIM55 function.
TRIM55 expression levels were significantly increased in GC cell lines and tissues. High expression of TRIM55 was correlated with poor prognosis of GC patients. Knockdown of TRIM55 in GC cell lines inhibited proliferation, colony formation, migration and invasion in vitro. TRIM55 can regulate the expression of epithelial-mesenchymal transition-related proteins in GC cells.
TRIM55 functions as an oncogene through promoting cell proliferation, migration and invasion in GC.
TRIM55 may be a new potential target in GC treatment.