Wu YL, Wang X, Du XX, Liu KL, Wang CF, Liu JC, Cao JM, Cui XL. Resveratrol suppresses ulcerative colitis and colitis-associated colorectal cancer via modulating the miR-31-5p/SATB2 axis. World J Gastrointest Oncol 2026; 18(11): 123558 [DOI: 10.4251/wjgo.123558]
Corresponding Author of This Article
Xiang-Li Cui, PhD, Full Professor, MOE Key Laboratory of Cellular Physiology, and Department of Physiology, Shanxi Medical University, No. 56 Xinjian South Road, Yingze District, Taiyuan 030001, Shanxi Province, China. cuixiangli@163.com
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Gastroenterology & Hepatology
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research-article
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Wu YL, Wang X, Du XX, Liu KL, Wang CF, Liu JC, Cao JM, Cui XL. Resveratrol suppresses ulcerative colitis and colitis-associated colorectal cancer via modulating the miR-31-5p/SATB2 axis. World J Gastrointest Oncol 2026; 18(11): 123558 [DOI: 10.4251/wjgo.123558]
World J Gastrointest Oncol. Nov 15, 2026; 18(11): 123558 Published online Nov 15, 2026. doi: 10.4251/wjgo.123558
Resveratrol suppresses ulcerative colitis and colitis-associated colorectal cancer via modulating the miR-31-5p/SATB2 axis
Ya-Li Wu, Xi Wang, Xin-Xin Du, Kai-Li Liu, Chun-Fang Wang, Jin-Chun Liu, Ji-Min Cao, Xiang-Li Cui
Ya-Li Wu, Xi Wang, Xin-Xin Du, Kai-Li Liu, Ji-Min Cao, Xiang-Li Cui, MOE Key Laboratory of Cellular Physiology, and Department of Physiology, Shanxi Medical University, Taiyuan 030001, Shanxi Province, China
Chun-Fang Wang, Experimental Animal Center, Shanxi Medical University, Taiyuan 030001, Shanxi Province, China
Jin-Chun Liu, Department of Gastroenterology, The First Hospital of Shanxi Medical University, Taiyuan 030001, Shanxi Province, China
Co-corresponding authors: Ji-Min Cao and Xiang-Li Cui.
Author contributions: Cui XL designed and coordinated the study; Liu JC provided the human ulcerative colitis samples used in this study; Wang CF provided miR-31 transgenic mice; Wu YL, Wang X, Liu KL, and Du XX performed experiments, acquired and analyzed data; Wu YL drafted manuscript, performed data analysis, and drew figures; Cao JM provided intellectual ideas on the study and revised manuscript; Cao JM and Cui XL contributed equally as co-corresponding authors. All authors approved the final version of the manuscript.
AI contribution statement: The author declares that no AI was used in the creation of the manuscript.
Supported by National Natural Science Foundation of China, No. 81272695.
Institutional review board statement: This study was approved by the Ethics Committee of Shanxi Medical University, No. 2016 LL014.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Ethics Committee of Shanxi Medical University, No. SYDL2026019.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Data sharing statement: All data in this study are available from the corresponding author upon reasonable request.
Corresponding author: Xiang-Li Cui, PhD, Full Professor, MOE Key Laboratory of Cellular Physiology, and Department of Physiology, Shanxi Medical University, No. 56 Xinjian South Road, Yingze District, Taiyuan 030001, Shanxi Province, China. cuixiangli@163.com
Received: May 22, 2026 Revised: July 13, 2026 Accepted: September 15, 2026 Published online: November 15, 2026 Processing time: 159 Days and 15.8 Hours
Core Tip
Core Tip: By integrating the microRNA sequencing data of human colorectal cancer from The Cancer Genome Atlas and the transcriptomic data from a small human ulcerative colitis (UC) cohort, we provisionally identify that miR-31-5p promotes the colonic inflammation-to-cancer transition. MiR-31-5p exacerbates dextran sulfate sodium-induced colitis and its transition to colitis-associated colorectal cancer (CAC) by targeting special AT-rich sequence-binding protein 2. The miR-31-5p/special AT-rich sequence-binding protein 2 axis is found to modulate Toll-like receptor-4/nuclear factor-κB and apoptosis pathways, revealing a key molecular link in UC-to-CAC transition. Resveratrol, a small plant-derived compound, ameliorates bowel inflammation and inhibits UC progression to CAC via this axis in mice in vivo. The study provides mechanistic insights into the UC-to-CAC progression and highlights the therapeutic potential of resveratrol for the diseases.
