Cai PY, Ma ML, Zhang YF, Zhou ZX, Wang Y, He LP, Wang W. Inhibition of glutathione metabolism can limit the development of pancreatic cancer. World J Stem Cells 2022; 14(5): 362-364 [PMID: 35722199 DOI: 10.4252/wjsc.v14.i5.362]
Corresponding Author of This Article
Wei Wang, MD, Attending Doctor, Department of Interventional Oncology, Municipal Hospital Affiliated to Taizhou University, No. 381-1 Zhongshan East Road, Jiaojiang District, Taizhou 318000, Zhejiang Province, China. westernfox000@163.com
Research Domain of This Article
Oncology
Article-Type of This Article
Letter to the Editor
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 Stem Cells. May 26, 2022; 14(5): 362-364 Published online May 26, 2022. doi: 10.4252/wjsc.v14.i5.362
Inhibition of glutathione metabolism can limit the development of pancreatic cancer
Pei-Yuan Cai, Mei-Lin Ma, Yang-Fen Zhang, Zi-Xuan Zhou, Yan Wang, Lian-Ping He, Wei Wang
Pei-Yuan Cai, Wei Wang, Department of Interventional Oncology, Municipal Hospital Affiliated to Taizhou University, Taizhou 318000, Zhejiang Province, China
Mei-Lin Ma, Yang-Fen Zhang, Zi-Xuan Zhou, Yan Wang, Lian-Ping He, School of Medicine, Taizhou University, Taizhou 318000, Zhejiang Province, China
Author contributions: Wang W and He LP contributed to conceptualization and formal analysis; Cai PY, Ma ML, Zhang YF, Wang Y, and Zhou ZX contributed to writing of the original draft, writing, reviewing, and editing; All authors participated in drafting the manuscript and have read, contributed to, and approved the final version of the manuscript.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
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: Wei Wang, MD, Attending Doctor, Department of Interventional Oncology, Municipal Hospital Affiliated to Taizhou University, No. 381-1 Zhongshan East Road, Jiaojiang District, Taizhou 318000, Zhejiang Province, China. westernfox000@163.com
Received: December 13, 2021 Peer-review started: December 13, 2021 First decision: March 13, 2022 Revised: March 15, 2022 Accepted: April 27, 2022 Article in press: April 27, 2022 Published online: May 26, 2022
Abstract
Pharmacological inhibitors of glutathione synthesis and circulation, such as buthionine-sulfoximine, inhibit glutathione metabolism. These drugs decrease the aggressiveness of pancreatic cancer, inhibit tumor stem cell survival, and reduce chemotherapy resistance. Nevertheless, buthionine-sulfoximine also decreases the content of glutathione in normal cells, disrupts the balance between reactive oxygen species and glutathione, and eventually induces cell apoptosis. Pancreatic cancer is usually diagnosed at an advanced stage and has a poor prognosis. Consequently, the use of biomarkers to screen high-risk patients can be an effective method.
Core Tip: To reduce side effects, pharmacological inhibitors of glutathione synthesis and circulation, such as buthionine-sulfoximine and 6-aminonicotinamide, can be assessed by in vivo models of pancreatic cancer. Evaluating the impact of different organs on metabolic processes and the invasiveness of cancer stem cells may provide new avenues for therapeutics targeting tumor metabolism.
