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©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Dec 15, 2025; 17(12): 112894
Published online Dec 15, 2025. doi: 10.4251/wjgo.v17.i12.112894
Published online Dec 15, 2025. doi: 10.4251/wjgo.v17.i12.112894
Novel insights into SLC16A8 in colorectal cancer
Jing-Yuan Li, Guang Ji, Yan-Qi Dang, Institute of Digestive Diseases, Longhua Hospital, China-Canada Center of Research for Digestive Diseases, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China
Author contributions: Dang YQ designed and revised the original draft; Ji G designed and edited the manuscript; Li JY wrote the original draft; all authors have read and approved the final manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
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: Yan-Qi Dang, PhD, Institute of Digestive Diseases, Longhua Hospital, China-Canada Center of Research for Digestive Diseases, Shanghai University of Traditional Chinese Medicine, Fenglin Road Sub-district, Shanghai 200032, China.
Received: August 8, 2025
Revised: September 12, 2025
Accepted: October 23, 2025
Published online: December 15, 2025
Processing time: 125 Days and 5.5 Hours
Revised: September 12, 2025
Accepted: October 23, 2025
Published online: December 15, 2025
Processing time: 125 Days and 5.5 Hours
Core Tip
Core Tip: Solute carrier family 16 member 8 (SLC16A8) drives the progression of the hypoxic microenvironment in colorectal cancer through dual mechanisms: Glycolytic reprogramming mediated by HIF-1α and endothelium-mesenchymal transition. Targeting SLC16A8 synergistically inhibits metabolic adaptation and vascular remodeling, demonstrating potential for clinical translation.