Basic Study
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Oncol. Apr 24, 2024; 15(4): 554-565
Published online Apr 24, 2024. doi: 10.5306/wjco.v15.i4.554
Regulation of TMEM100 expression by epigenetic modification, effects on proliferation and invasion of esophageal squamous carcinoma
Yue-Feng Xu, Yan Dang, Wei-Bo Kong, Han-Lin Wang, Xiu Chen, Long Yao, Yuan Zhao, Ren-Quan Zhang
Yue-Feng Xu, Yan Dang, Wei-Bo Kong, Han-Lin Wang, Xiu Chen, Long Yao, Yuan Zhao, Ren-Quan Zhang, Department of Thoracic Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei 230000, Anhui Province, China
Author contributions: Xu YF and Dang Y are responsible for data curation and writing (original draft preparation); Kong WB is responsible for visualisation; Wang HL and Chen X are responsible for software and validation; Zhao Y is responsible for methodology; Yao L is responsible for writing (reviewing and editing); Zhang RQ is responsible for conceptualization and resources.
Institutional review board statement: This study does not involve human subjects.
Institutional animal care and use committee statement: This study does not involve animal subjects.
Conflict-of-interest statement: No conflicts of interest are associated with any of the senior authors or other co-authors who contributed their efforts to this manuscript.
Data sharing statement: Technical appendix, statistical code, and dataset available from the corresponding author at a1285624638@163.com
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: Ren-Quan Zhang, MD, Surgeon, Department of Thoracic Surgery, The First Affiliated Hospital of Anhui Medical University, No. 218 Ji Xi Road, Hefei 230000, Anhui Province, China. zhangrenquanayfy@163.com
Received: January 2, 2024
Peer-review started: January 2, 2024
First decision: January 20, 2024
Revised: February 1, 2024
Accepted: March 20, 2024
Article in press: March 20, 2024
Published online: April 24, 2024
Processing time: 111 Days and 7.8 Hours
ARTICLE HIGHLIGHTS
Research background

TMEM100 is associated with multiple malignancies but its role in esophageal squamous cell carcinoma (ESCC) remains unknown.

Research motivation

This study aimed to investigate the regulatory mechanism of TMEM100 expression in ESCC and its effect on ESCC cell growth and proliferation.

Research objectives

This study hopes to clarify the role of TMEM100 in ESCC as well as to preliminarily investigate the epigenetic regulation of TMEM100 expression.

Research methods

We used R software and online analysis databases to analyze the expression, prognosis and pathway of TMEM100 in esophageal cancer (EC). Utilization of real-time PCR and western blotting to probe the expression of TMEM100 and pathway proteins in ESCC. In addition, the effects of TMEM100 overexpression on the proliferation, invasion and migration of ESCC cells were assessed by CCK-8 and clone formation assays.

Research results

Kaplan-meier survival analysis revealed that low expression of TMEM100 correlated with poor prognosis in patients with EC. Further, treatment with the demethylating agent 5-AZA resulted in increased TMEM100 expression in ESCC cells. Additionally, TMEM100 overexpression exhibited inhibitory effects on the proliferation, invasion, and migration of ESCC cells. Enrichment analysis highlighted significant enrichment in the mitogen-activated protein kinases (MAPK) signalling pathway, which was validated using western blotting, confirming TMEM100’s involvement in the regulation of the MAPK signalling pathway in ESCC cells.

Research conclusions

TMEM100 is highly expressed in normal subjects and lowly expressed in EC patients, and patients with high TMEM100 expression in EC patients have a better prognosis. The expression of TMEM100 was increased in ESCC cells treated with the methylation inhibitor 5-AZA. Overexpression of TMEM100 gene inhibited the growth and proliferation of ESCC cells and negatively regulated the MAPK signaling pathway.

Research perspectives

The robustness of TMEM100 as a prognostic indicator for ESCC needs to be further validated. Further clarification of the in vivo effects of overexpression of TMEM100 on the proliferation of esophageal squamous carcinoma is needed.