Basic Study
Copyright ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Oct 15, 2022; 14(10): 1949-1967
Published online Oct 15, 2022. doi: 10.4251/wjgo.v14.i10.1949
Overexpression of ELL-associated factor 2 suppresses invasion, migration, and angiogenesis in colorectal cancer
Ming-Liang Feng, Can Wu, Hui-Jing Zhang, Huan Zhou, Tai-Wei Jiao, Meng-Yuan Liu, Ming-Jun Sun
Ming-Liang Feng, Can Wu, Hui-Jing Zhang, Huan Zhou, Tai-Wei Jiao, Meng-Yuan Liu, Ming-Jun Sun, Department of Endoscopy, The First Hospital Affiliated to China Medical University, Shenyang 110001, Liaoning Province, China
Author contributions: Feng ML and Wu C designed the research study; Zhang HJ and Jiao TW performed the research; Zhou H and Liu MY contributed new reagents and analytic tools; Feng ML and Sun MJ analyzed the data and wrote the manuscript; and all authors have read and approved the final manuscript.
Supported by the Natural Science Foundation of Liaoning Province, No. 2019-BS-279.
Institutional review board statement: This study was approved by the Institutional Review Board of The First Affiliated Hospital of China Medical University (Registration No. 2021-68-2).
Informed consent statement: Patients were not required to give informed consent to the study because the analysis used anonymous data that were obtained after each patient agreed to treatment by written consent.
Conflict-of-interest statement: All the authors report no relevant conflicts 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: Ming-Jun Sun, Doctor, PhD, Chief Physician, Professor, Department of Endoscopy, The First Hospital Affiliated to China Medical University, No. 155 Nanjing North Street, Shenyang 110001, Liaoning Province, China. sunydyy@163.com
Received: May 19, 2022
Peer-review started: May 19, 2022
First decision: June 6, 2022
Revised: June 20, 2022
Accepted: September 21, 2022
Article in press: September 21, 2022
Published online: October 15, 2022
ARTICLE HIGHLIGHTS
Research background

There are few studies on the expression and role of ELL-associated factor 2 (EAF2) protein in colorectal cancer (CRC). The molecular mechanism of involvement of EAF2 in CRC invasion and metastasis remains unclear.

Research motivation

EAF2 may play a tumor suppressive and protective role in the development of CRC by inhibiting the invasion, metastasis, and angiogenesis of CRC cells.

Research objectives

We assessed the expression and localization of EAF2 protein in CRC specimens. Meanwhile, we cultured CRC cells in vitro to determine the expression of EAF2 protein and further investigate its effects on the biological function of CRC cells.

Research methods

We used immunohistochemistry and western blot assay to detect the expression of EAF2 protein in CRC tissues from 70 patients. In addition, we applied plasmid transfection technology to study the effects of EAF2 on the invasion, migration, and angiogenesis of CRC cells in vitro.

Research results

EAF2 protein was lowly expressed in cancer tissues of patients with advanced CRC. Kaplan-Meier survival analysis showed that the survival rate of the group with high EAF2 level was higher than that of the group with low EAF2 level. In addition, EAF2 affected the biological functions of CRC cells by regulating the STAT3/TGF-β1 crosstalk pathway.

Research conclusions

As a tumor suppressor, EAF2 may play a tumor suppressive and protective role in the development of CRC by inhibiting the invasion, metastasis, and angiogenesis of CRC cells via regulating the signal transducer and activator of transcription 3/transforming growth factor beta 1 crosstalk pathway. These findings may provide new diagnostic markers and novel therapeutic targets for CRC.

Research perspectives

Our data is beneficial to elucidate the molecular mechanism of CRC invasion and metastasis as well as explore new potential molecular markers and the direction of targeted therapy.