Progress in Prevention and Treatment of Dysplasia in Ulcerative Colitis Based on Cyclooxygenase-2/p53 Axis.
10.3881/j.issn.1000-503X.15911
- Author:
Yi-Lin ZHANG
1
;
Shu-Sen YANG
1
;
Yu-Shan LIU
1
;
Shu-Guang YAN
1
Author Information
1. Basic Medical College of Shaanxi University of Chinese Medicine,Xianyang,Shaanxi 712046,China.
- Publication Type:Review
- Keywords:
cyclooxygenase-2;
dysplasia;
p53 gene;
ulcerative colitis
- MeSH:
Colitis, Ulcerative/metabolism*;
Humans;
Cyclooxygenase 2/metabolism*;
Tumor Suppressor Protein p53/metabolism*;
Intestinal Mucosa/metabolism*;
Apoptosis;
Cell Proliferation
- From:
Acta Academiae Medicinae Sinicae
2024;46(6):940-948
- CountryChina
- Language:English
-
Abstract:
Ulcerative colitis(UC)is a chronic inflammatory bowel disease characterized by non-specific,persistent inflammation in the intestines.This chronic inflammation often increases the risk of serious complications such as colorectal cancer.Dysplasia acts as a driver of cancer development and plays a connecting role in the occurrence and development of chronic intestinal inflammation and colorectal cancer.Cell proliferation/apoptosis imbalance is the driving factor for dysplasia development.The abnormal proliferation/apoptosis of intestinal mucosal epithelial cells may be affected by cyclooxygenase-2(COX-2),tumor suppressor gene p53,or both.Therefore,reasonable regulation of COX-2/p53 axis may be a key to achieving intestinal mucosal proliferation/apoptosis balance.This article discusses the effects and mechanism of COX-2 and p53 in regulating the occurrence and development of dysplasia in UC from the proliferation/apoptosis imbalance of intestinal mucosal epithelial cells,aiming to provide a reference for understanding the mechanism of dysplasia in UC and developing targeted therapeutic drugs.
