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 of FBXL6 in the proliferation and epithelial-mesenchymal transition (EMT) of gastric cancer (GC) remains to be investigated.
To investigate the effect of FBXL6 on the proliferation of GC cells and to find new therapeutic targets for the treatment of GC.
The present study to clarify the effect of FBXL6 on the prognosis of GC patients and the proliferation and EMT of GC cells.
The expression of FBXL6 expression in GC tissues and cells was detected using RT-qPCR and Western blotting. In vitro, stable FBXL6 knockdown and overexpressed GC cell lines were cultured, and the proliferation, clone formation, migration and invasion ability of GC cells were examined using cholecystokinin-8 assay, clone formation assay, wound healing assay and transwell assay, respectively. In vivo tumor assays were performed to prove whether FBXL6 promoted cell proliferation in vivo. Western blotting was used to detect the association of FBXL6 protein with EMT-related protein expression levels.
FBXL6 expression is elevated in GC cells and tissues, and FBXL6 expression levels correlated with histological grade, pathological stage, T grade, and tumor size. In vitro, endogenous silenced of FBXL6 suppressed GC cell proliferation, migration, invasion and EMT. In vivo, knockdown of FBXL6 inhibited subcutaneous graft tumor growth in nude mice.
FBXL6 expression is increased in GC tissues and cell lines. FBXL6 promotes the proliferation migration, invasion, and epithelial-mesenchymal transition of GC cells.
FBXL6 may have potential as an important prognostic indicator and therapeutic destination for GC. Further search for potential cancer-promoting mechanisms of FBXL6 is needed in the future.