Basic Study
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Oncol. Feb 24, 2024; 15(2): 302-316
Published online Feb 24, 2024. doi: 10.5306/wjco.v15.i2.302
TM9SF1 promotes bladder cancer cell growth and infiltration
Long Wei, Shi-Shuo Wang, Zhi-Guang Huang, Rong-Quan He, Jia-Yuan Luo, Bin Li, Ji-Wen Cheng, Kun-Jun Wu, Yu-Hong Zhou, Shi Liu, Sheng-Hua Li, Gang Chen
Long Wei, Ji-Wen Cheng, Kun-Jun Wu, Yu-Hong Zhou, Shi Liu, Sheng-Hua Li, Department of Urology, First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
Shi-Shuo Wang, Zhi-Guang Huang, Jia-Yuan Luo, Bin Li, Gang Chen, Department of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
Rong-Quan He, Department of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
Author contributions: Wang SS, He RQ, Cheng JW, Li SH, and Chen G conceived and designed the study; Wei L, Wang SS, Luo JY, Li B, Wu KJ, Zhou YH, and Liu S performed the experiments, and acquired and analyzed the data; Wei L, Wang SS, and Huang ZG wrote the manuscript; He RQ, Luo JY, Li B, Cheng JW, Li SH, and Chen G revised and corrected the draft; all authors approved the final version of the article.
Supported by National Natural Science Foundation of China, No. 82260785.
Institutional review board statement: The study did not involve human or animal subjects.
Institutional animal care and use committee statement: The study did not involve animal experiments.
Conflict-of-interest statement: All authors declare no conflict of interest for this article.
Data sharing statement: No additional data are available.
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: Gang Chen, MD, PhD, Full Professor, Department of Pathology, First Affiliated Hospital of Guangxi Medical University, No. 22 Shuangyong Road, Nanning 530021, Guangxi Zhuang Autonomous Region, China. chengang@gxmu.edu.cn
Received: September 15, 2023
Peer-review started: September 15, 2023
First decision: October 17, 2023
Revised: October 20, 2023
Accepted: November 27, 2023
Article in press: November 27, 2023
Published online: February 24, 2024
Processing time: 157 Days and 22.8 Hours
Abstract
BACKGROUND

Bladder cancer (BC) is the most common urological tumor. It has a high recurrence rate, displays tutor heterogeneity, and resists chemotherapy. Furthermore, the long-term survival rate of BC patients has remained unchanged for decades, which seriously affects the quality of patient survival. To improve the survival rate and prognosis of BC patients, it is necessary to explore the molecular mechanisms of BC development and progression and identify targets for treatment and intervention. Transmembrane 9 superfamily member 1 (TM9SF1), also known as MP70 and HMP70, is a member of a family of nine transmembrane superfamily proteins, which was first identified in 1997. TM9SF1 can be expressed in BC, but its biological function and mechanism in BC are not clear.

AIM

To investigate the biological function and mechanism of TM9SF1 in BC.

METHODS

Cells at 60%-80% confluence were transfected with lentiviral vectors for 48-72 h to achieve stable TM9SF1 overexpression or silencing in three BC cell lines (5637, T24, and UM-UC-3). The effect of TM9SF1 on the biological behavior of BC cells was then investigated through CCK8, wound-healing assay, transwell assay, and flow cytometry.

RESULTS

Overexpression of TM9SF1 increased the in vitro proliferation, migration, and invasion of BC cells by promoting the entry of BC cells into the G2/M phase. Silencing of TM9SF1 inhibited in vitro proliferation, migration, and invasion of BC cells and blocked BC cells in the G1 phase.

CONCLUSION

TM9SF1 may be an oncogene in BC.

Keywords: TM9SF1; Bladder cancer; Biological function; Cell function assay; Oncogene

Core Tip: This study was the first to attempt to construct a stable bladder cancer (BC) cell line to investigate the overexpression and silencing of transmembrane 9 superfamily member 1 (TM9SF1) using in vitro experiments for the purpose of exploring the pro-cancer effect of TM9SF1 in BC. We verified that overexpression of TM9SF1 could enhance the growth, migration, and invasion of BC cells and promote their entry into G2/M phase of the cell cycle. This information not only provides a new target in developing treatments for BC but is also a source of hope for BC patients.