Xue XJ, Li FR, Yu J. Mitochondrial pathway of the lysine demethylase 5C inhibitor CPI-455 in the Eca-109 esophageal squamous cell carcinoma cell line. World J Gastroenterol 2021; 27(16): 1805-1815 [PMID: 33967558 DOI: 10.3748/wjg.v27.i16.1805]
Corresponding Author of This Article
Jing Yu, PhD, Doctor, Department of Laboratory Medicine, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 116 Zhuodaoquan South Road, Wuhan 430079, Hubei Province, China. yujings9774@sina.com.cn
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 Gastroenterol. Apr 28, 2021; 27(16): 1805-1815 Published online Apr 28, 2021. doi: 10.3748/wjg.v27.i16.1805
Mitochondrial pathway of the lysine demethylase 5C inhibitor CPI-455 in the Eca-109 esophageal squamous cell carcinoma cell line
Xiao-Jie Xue, Fei-Rong Li, Jing Yu
Xiao-Jie Xue, Fei-Rong Li, Department of Clinical Laboratory, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Edong Healthcare Group, Huangshi 435000, Hubei Province, China
Xiao-Jie Xue, Hubei Key Laboratory of Kidney Disease Pathogenesis and Intervention, Huangshi 435000, Hubei Province, China
Xiao-Jie Xue, Medical College, Wuhan University of Science and Technology, Wuhan 430081, Hubei Province, China
Jing Yu, Department of Laboratory Medicine, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430079, Hubei Province, China
Author contributions: Xue XJ analyzed the data, drafted the article, and contributed to study design; Li FR contributed to data gathering; Yu J contributed to study design, editing, and revising the paper; all authors read and approved the final manuscript.
Supported byYoung Talents Project of Hubei Provincial Health Commission, No. WJ2019H449.
Institutional review board statement: The study was reviewed and approved by Hubei cancer hospital, Tongji Medical College, Huazhong University of Science and Technology (approval No. LLHBCH2020LW-027).
Conflict-of-interest statement: The authors declare that they have no competing interests..
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: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Jing Yu, PhD, Doctor, Department of Laboratory Medicine, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 116 Zhuodaoquan South Road, Wuhan 430079, Hubei Province, China. yujings9774@sina.com.cn
Received: January 8, 2021 Peer-review started: January 8, 2021 First decision: February 11, 2021 Revised: February 14, 2021 Accepted: March 24, 2021 Article in press: March 24, 2021 Published online: April 28, 2021 Processing time: 102 Days and 17.6 Hours
ARTICLE HIGHLIGHTS
Research background
Esophageal cancer is a malignant tumor of the digestive tract that is difficult to diagnose early. Although CPI-455 is reported to inhibit various cancers, the role of CPI-455 in esophageal squamous cell carcinoma (ESCC) is unknown.
Research motivation
KDM5C, a lysine-specific demethylase 5C, inhibited ESCC proliferation and invasion, which may be partly associated with the expression of p53, Bax, Caspase-9, and Caspase-3. Mitochondria-mediated intrinsic apoptotic signaling plays an important role in the process of Eca-109 cell apoptosis induced by CPI-455.
Research objectives
The study objective was to investigate the effect and mechanism of the KDM5C inhibitor, CPI-455, on ESCC cells.
Research methods
The changes in proliferation, apoptosis, ROS content, and mitochondrial membrane potential of Eca-109 cells induced by CPI-455 were observed. The expression of P53, Bax, Caspase-9, Caspase-3, and KDM5C in Eca-109 cells was assayed.
Research results
CPI-455 inhibited Eca-109 cell proliferation. P53, Bax, Caspase-9, and Caspase-3 were upregulated in Eca-109 cells, and KDM5C was significantly downregulated, by CPI-455. CPI-455 increased the level of intracellular ROS in Eca-109 cells, and decreased the mitochondrial membrane potential compared with the control group.
Research conclusions
CPI-455 inhibited Eca-109 cell proliferation via the mitochondrial apoptosis pathway by regulating the expression of related genes.
Research perspectives
CPI-455 might be a potential candidate for the development of novel chemotherapeutic agents to treat ESCC.
