Abstract

Gastric cancer (GC) is considered a major global health problem. The role of TRIM55, a member of the three-domain protein family, in GC is unknown. To determine the expression of TRIM55 in GC tissues and its relationship with clinicopathological characteristics, and to investigate the effects of TRIM55 on the malignant biological behavior of GC cells. Differential expression of TRIM55 in GC and para-cancer tissues was detected by immunohistochemistry, and the relationship between TRIM55 level and clinicopathological characteristics and prognosis was analyzed. Gain-of-function, loss-of-function, cell counting kit-8 assay, colony formation, transwell assay, wound healing assay, and western blot analysis were used to assess the potential role of TRIM55 in the development of GC. TRIM55 expression was significantly increased in GC tissues compared with adjacent normal tissues. High expression of TRIM55 was associated with advanced pathological stage and poor prognosis. Overexpression of TRIM55 promoted invasion and metastasis of GC cells in vitro by regulating epithelial-mesenchymal transition (EMT), whereas knockdown of TRIM55 had the opposite effect. Our data showed that TRIM55 is highly expressed in GC tissues, and is associated with poor prognosis. TRIM55 plays the role of an oncogene in GC, and it promotes metastasis of GC through the regulation of EMT. TRIM55 may be a possible target for the diagnosis and prognosis of GC patients.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

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.