Basic Study
Copyright ©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Mar 15, 2023; 15(3): 490-503
Published online Mar 15, 2023. doi: 10.4251/wjgo.v15.i3.490
F-box and leucine-rich repeat 6 promotes gastric cancer progression via the promotion of epithelial-mesenchymal transition
Lei Meng, Yu-Ting Hu, A-Man Xu
Lei Meng, A-Man Xu, Department of General Surgery, First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui Province, China
Yu-Ting Hu, Department of Immunology, College of Basic Medicine, Anhui Medical University, Hefei 230022, Anhui Province, China
Author contributions: Meng L collected the data and wrote the manuscript; Hu YT participated in the discussion; Xu AM reviewed the manuscript and provided funding support; all authors contributed to the article and approved the submitted version.
Supported by the Key Research and Development Program of Anhui Province, No. 202104J07020029.
Institutional review board statement: The study was reviewed and approved by the Institutional Review Board of the First Affiliated Hospital of Anhui Medical University (Approval No. Quick PJ 2019-10-11).
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by Anhui Medical University Laboratory Animal Ethics Committee (Approval No. LLSC20200513).
Informed consent statement: All study participants, or their legal guardian, provided informed written consent prior to study enrollment.
Conflict-of-interest statement: There is no conflict of interest in this study.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE Guidelines, and the manuscript was prepared and revised according to the ARRIVE Guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: A-Man Xu, Doctor, PhD, Chief Physician, Full Professor, Department of General Surgery, First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Avenue, Shushan District, Hefei 230022, Anhui Province, China. amanxu1965@163.com
Received: December 4, 2022
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
ARTICLE HIGHLIGHTS
Research background

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.

Research motivation

To investigate the effect of FBXL6 on the proliferation of GC cells and to find new therapeutic targets for the treatment of GC.

Research objectives

The present study to clarify the effect of FBXL6 on the prognosis of GC patients and the proliferation and EMT of GC cells.

Research methods

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.

Research results

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.

Research conclusions

FBXL6 expression is increased in GC tissues and cell lines. FBXL6 promotes the proliferation migration, invasion, and epithelial-mesenchymal transition of GC cells.

Research perspectives

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.