Published online Mar 15, 2023. doi: 10.4251/wjgo.v15.i3.490
Peer-review started: December 4, 2022
First decision: December 24, 2022
Revised: January 6, 2023
Accepted: February 14, 2023
Article in press: February 14, 2023
Published online: March 15, 2023
Processing time: 100 Days and 12.4 Hours
F-box and leucine-rich repeat 6 (FBXL6) have reportedly been associated with several cancer types. However, the role and mechanisms of FBXL6 in gastric cancer (GC) require further elucidation.
To investigate the effect of FBXL6 in GC tissues and cells and the underlying mechanisms.
TCGA and GEO database analysis was performed to evaluate the expression of FBXL6 in GC tissues and adjacent normal tissues. Reverse transcription-quan
FBXL6 expression was upregulated more in tumor tissues than in adjacent normal tissues and positively associated with clinicopathological characteristics. The outcomes of CCK-8, clone formation, and Edu assays demonstrated that FBXL6 knockdown inhibited cell proliferation, whereas upregulation of FBXL6 promoted proliferation in GC cells. Additionally, the transwell migration assay revealed that FBXL6 knockdown suppressed migration and invasion, whereas the overexpression of FBXL6 showed the opposite results. Through the subcutaneous tumor implantation assay, it was evident that the knockdown of FBXL6 inhibited GC graft tumor growth in vivo. Western blotting showed that the effects of FBXL6 on the expression of the proteins associated with the epithelial-mesenchymal transition-associated proteins in GC cells.
Silencing of FBXL6 inactivated the EMT pathway to suppress GC malignancy in vitro. FBXL6 can potentially be used for the diagnosis and targeted therapy of patients with GC.
Core Tip: F-box and leucine-rich repeat 6 (FBXL6) is up-regulated in gastric cancer (GC) cell lines and tissues, which is correlated with tumor size, grade of differentiation, and TNM stage. Knockdown of TRIM55 in GC cells suppressed proliferation, migration and invasion of cells and affected the expression of cell epithelial-mesenchymal transition-related proteins. Our study provides novel evidence that FBXL6 contributes the growth and metastasis of GC.