Hao WW, Xu F. KIFC3 promotes proliferation, migration and invasion of esophageal squamous cell carcinoma cells by activating EMT and β-catenin signaling. World J Gastrointest Oncol 2022; 14(7): 1239-1251 [PMID: 36051093 DOI: 10.4251/wjgo.v14.i7.1239]
Corresponding Author of This Article
Feng Xu, MD, Chief Doctor, Professor, Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Road, Zhengzhou 450052, Henan Province, China. xufengmd@sina.com
Research Domain of This Article
Oncology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastrointest Oncol. Jul 15, 2022; 14(7): 1239-1251 Published online Jul 15, 2022. doi: 10.4251/wjgo.v14.i7.1239
KIFC3 promotes proliferation, migration and invasion of esophageal squamous cell carcinoma cells by activating EMT and β-catenin signaling
Wei-Wei Hao, Feng Xu
Wei-Wei Hao, Feng Xu, Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China
Author contributions: Hao WW designed and performed experiments, analyzed data, and wrote the article; Xu F conceived the study, analyzed the data, and revised the article; all authors have read and approved the final manuscript.
Institutional review board statement: The study was reviewed and approved by the Institutional Review Board at the First Hospital of Zhengzhou University (No. 2021-KY-0446-001).
Institutional animal care and use committee statement: All animal research procedures were approved by the Ethics Committee of the First Affiliated Hospital of Zhengzhou University (No. 2021-KY-0446-001). All animal experiments were carried out in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals (NIH Publications No. 8023, revised 1978).
Conflict-of-interest statement: The authors declare no conflicts of interest.
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: Feng Xu, MD, Chief Doctor, Professor, Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Road, Zhengzhou 450052, Henan Province, China. xufengmd@sina.com
Received: November 18, 2021 Peer-review started: November 18, 2021 First decision: January 12, 2022 Revised: January 26, 2022 Accepted: March 26, 2022 Article in press: March 26, 2022 Published online: July 15, 2022 Processing time: 236 Days and 15.7 Hours
ARTICLE HIGHLIGHTS
Research background
Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies. The mechanism of ESCC is still unclear.
Research motivation
Kinesin family member (KIF)C3 has microtubule motor activity and may be involved in mitotic progression. KIFC3 was also shown to be involved in cell invasion and migration, as well as in survival, in hepatocellular carcinoma.
Research objectives
To elucidate the role of KIFC3 in ESCC and the underlying mechanisms.
Research methods
The expression of KIFC3 was evaluated in ESCC tissues and normal tissues. In addition, KIFC3 knockdown and KIFC3-overexpressing cell lines were constructed and then colony formation, EdU assays, cell cycle analysis, Transwell assays, and western blotting were performed to explore the underlying mechanisms of action. A xenograft tumor model in nude mice was used to verify the role of KIFC3 in tumorigenesis.
Research results
We showed that KIFC3 was upregulated in ESCC tissues and was associated with poor prognosis. KIFC3 promoted cell proliferation, mitosis progression, migration and invasion. In addition, KIFC3 knockdown suppressed ESCC tumorigenesis in an in vivo model. Mechanistically, we validated the involvement of KIFC3 β-catenin signaling and epithelial–mesenchymal transition (EMT) in ESCC progression.
Research conclusions
We found that KIFC3 was overexpressed in ESCC, and the expression of this protein was associated with prognosis in ESCC patients. Furthermore, KIFC3 promoted proliferation, migration, and invasion of ESCC via β-catenin signaling and EMT.
Research perspectives
Although the detailed mechanism underlying the effect of KIFC3 in promoting ESCC progression should be studied more carefully in our next research, we believe our research strongly suggests that KIFC3 may be a potential new therapeutic target for ESCC treatment.
