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World J Gastrointest Oncol. Oct 15, 2026; 18(10): 119879
Published online Oct 15, 2026. doi: 10.4251/wjgo.119879
Published online Oct 15, 2026. doi: 10.4251/wjgo.119879
Enterocloster bolteae drives hyperglycemia-associated colorectal cancer cell proliferation via Rac/Rho-MSH6-Elongin C signaling pathway
Yu Lai, Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Gastroenterology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, Guangdong Province, China
Ji-Hao Xu, Hong Luo, Ying Lin, Yun-Fang Yu, Qi-Kui Chen, Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Guangdong-Hong Kong Joint Laboratory for RNA Medicine, Department of Gastroenterology, Department of Medical Oncology, Department of Clinical Laboratory, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, Guangdong Province, China
Yong-Jian Chen, Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institute, Stockholm 111 29, Sweden
Ying Lin, Department of Gastroenterology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, Guangdong Province, China
Yun-Fang Yu, Guangdong Provincial Key Laboratory of Cancer Pathogenesis and Precision Diagnosis and Treatment, Shenshan Medical Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Shanwei 516600, Guangdong Province, China
Co-first authors: Yu Lai and Ji-Hao Xu.
Author contributions: Lai Y and Xu JH managed project administration, and they contributed equally to this article as co-first authors; Lai Y and Chen YJ performed software operation, data curation, and formal analysis; Lai Y and Luo H performed validation and investigation; Lai Y and Yu YF conceptualized the work, developed the methodology, provided resources, and prepared the original draft; Chen YJ and Lin Y reviewed and edited the manuscript; Lin Y was responsible for visualization and supervision; Xu JH, Yu YF, and Chen QK acquired funding; and all authors read and agreed to the published version of the manuscript.
AI contribution statement: The main text of the “Answering-Reviewers” document was not generated by AI, and the document contained no images. No AI tools participated in design of the study or interpretation of its results. However, the AI tool DeepSeek was used solely for language polishing and translation.
Supported by the National Natural Science Foundation of China, No. 81970464; the National Natural Science Foundation of Guangdong Province, No. 2022A1515110529; and Guangdong Science and Technology Department, No. 2024B1212030002.
Institutional review board statement: This study was approved by the Medical Ethics Committee of Sun Yat-sen Memorial Hospital, Sun Yat-sen University, approval No. 2021.174.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: The data that support the findings of this study are available from the corresponding author upon reasonable request.
Corresponding author: Ying Lin, MD, PhD, Department of Gastroenterology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, No. 107 Yanjiang Xi Road, Guangzhou 510120, Guangdong Province, China. linwy@mail.sysu.edu.cn.
Received: February 27, 2026
Revised: March 19, 2026
Accepted: May 13, 2026
Published online: October 15, 2026
Processing time: 200 Days and 19.1 Hours
Revised: March 19, 2026
Accepted: May 13, 2026
Published online: October 15, 2026
Processing time: 200 Days and 19.1 Hours
Core Tip
Core Tip: Diabetes mellitus is an established independent risk factor for colorectal cancer (CRC). We identified Enterocloster bolteae as a discriminative gut microbial signature specific to patients with diabetes mellitus and CRC. Functional pathway analysis further revealed distinctive enrichment of a carcinogenesis-related signaling pathway in this cohort, which included RAC, RHO, MSH6, and Elongin C, and this finding was subsequently validated in vitro. These findings establish a link between a diabetes-enriched gut bacterium and the activation of oncogenic pathways in CRC.