Liu YP, Qiu ZZ, Li XH, Li EY. Propofol induces ferroptosis and inhibits malignant phenotypes of gastric cancer cells by regulating miR-125b-5p/STAT3 axis. World J Gastrointest Oncol 2021; 13(12): 2114-2128 [PMID: 35070046 DOI: 10.4251/wjgo.v13.i12.2114]
Corresponding Author of This Article
En-You Li, PhD, Chief Physician, Department of Anesthesiology, First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng Street, Nangang District, Harbin 150001, Heilongjiang Province, China. enyouli@sina.com
Research Domain of This Article
Gastroenterology & Hepatology
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. Dec 15, 2021; 13(12): 2114-2128 Published online Dec 15, 2021. doi: 10.4251/wjgo.v13.i12.2114
Propofol induces ferroptosis and inhibits malignant phenotypes of gastric cancer cells by regulating miR-125b-5p/STAT3 axis
Yi-Ping Liu, Zhong-Zhi Qiu, Xu-Hui Li, En-You Li
Yi-Ping Liu, Zhong-Zhi Qiu, En-You Li, Department ofAnesthesiology, First Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang Province, China
Xu-Hui Li, Department of Gastroenterology, Heilongjiang Forest Industry Federation (Red Cross) Hospital, Harbin 150008, Heilongjiang Province, China
Author contributions: Liu YP and Qiu ZZ designed the study; Liu YP and Li XH performed the experiments; Qiu ZZ collected and analyzed data; Li EY wrote the manuscript.
Institutional review board statement: This study was reviewed and approved by the Ethics Committee of the First Affiliated Hospital of Harbin Medical University.
Institutional animal care and use committee statement: All animal experiments were performed under the approval of Animal Ethics Committee of The First Affiliated Hospital of Harbin Medical University.
Conflict-of-interest statement: The authors declare no conflict 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: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: En-You Li, PhD, Chief Physician, Department of Anesthesiology, First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng Street, Nangang District, Harbin 150001, Heilongjiang Province, China. enyouli@sina.com
Received: July 6, 2021 Peer-review started: July 6, 2021 First decision: July 26, 2021 Revised: September 10, 2021 Accepted: October 25, 2021 Article in press: October 25, 2021 Published online: December 15, 2021
Abstract
BACKGROUND
Gastric cancer is a common malignancy with poor prognosis, in which ferroptosis plays a crucial function in its development. Propofol is a widely used anesthetic and has antitumor potential in gastric cancer. However, the effect of propofol on ferroptosis during gastric cancer progression remains unreported.
AIM
To explore the function of propofol in the regulation of ferroptosis and malignant phenotypes of gastric cancer cells.
METHODS
MTT assays, colony formation assays, Transwell assays, wound healing assay, analysis of apoptosis, ferroptosis measurement, luciferase reporter gene assay, and quantitative reverse transcription polymerase chain reaction were used in this study.
RESULTS
Our data showed that propofol was able to inhibit proliferation and induce apoptosis of gastric cancer cells. Meanwhile, propofol markedly repressed the invasion and migration of gastric cancer cells. Importantly, propofol enhanced the erastin-induced inhibition of growth of gastric cancer cells. Consistently, propofol increased the levels of reactive oxygen species, iron, and Fe2+ in gastric cancer cells. Moreover, propofol suppressed signal transducer and activator of transcription (STAT)3 expression by upregulating miR-125b-5p and propofol induced ferroptosis by targeting STAT3 in gastric cancer cells. The miR-125b-5p inhibitor or STAT3 overexpression reversed propofol-attenuated malignant phenotypes of gastric cancer cells.
CONCLUSION
Propofol induced ferroptosis and inhibited malignant phenotypes of gastric cancer cells by regulating the miR-125b-5p/STAT3 axis. Propofol may serve as a potential therapeutic candidate for gastric cancer.
Core Tip: In this study, we discovered that propofol induced ferroptosis and inhibited malignant phenotypes of gastric cancer cells by regulating the miR-125b-5p/STAT3 axis. Propofol may serve as a potential therapeutic candidate for gastric cancer.
