Evidence map›Paper›PMID 42892644›Full record

ArticleBritish journal of cancer2026

CXCL14+ fibroblasts promote development of IBD-associated fibrosis and cancer by interacting with SPP1+ macrophages via collagen IV secretion.

Haonan Zhang, Yulu Shi, Qiuyu Song, Na Li, Zhaoxian Lin, Qiusan Chen, Yi Yang, Yanjun Chen, Qian Liu, Yan Tan and 7 more

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In one paragraph

Article in British journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

17 authors.

Haonan Zhang *Department of Gastroenterology; Guangdong Provincial Key Laboratory of Major Obstetric Diseases; Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology; The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Yulu Shi *Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Qiuyu Song *Department of Gastroenterology; Guangdong Provincial Key Laboratory of Major Obstetric Diseases; Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology; The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Na LiDepartment of Gastroenterology, Guangxi Liuzhou Worker's Hospital, Liuzhou, China.
Zhaoxian LinDepartment of Gastroenterology; Guangdong Provincial Key Laboratory of Major Obstetric Diseases; Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology; The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Qiusan ChenDepartment of Gastroenterology; Guangdong Provincial Key Laboratory of Major Obstetric Diseases; Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology; The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Yi YangDepartment of Gastroenterology; Guangdong Provincial Key Laboratory of Major Obstetric Diseases; Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology; The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Yanjun ChenDepartment of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Qian LiuNanfang Hospital (The First School of Clinical Medicine), Southern Medical University, Guangzhou, China.
Yan TanDepartment of Gastroenterology, The First Affiliated Hospital, Hainan Medical University, Haikou, China.
Yifeng ZhengDepartment of Gastroenterology; Guangdong Provincial Key Laboratory of Major Obstetric Diseases; Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology; The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Shanping WangDepartment of Gastroenterology; Guangdong Provincial Key Laboratory of Major Obstetric Diseases; Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology; The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Yan SunDepartment of Gastroenterology; Guangdong Provincial Key Laboratory of Major Obstetric Diseases; Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology; The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Xiaxi LiDepartment of Gastroenterology, Shenzhen Hospital of Southern Medical University, Shenzhen, China.
Chengcheng HeDepartment of Gastroenterology; Guangdong Provincial Key Laboratory of Major Obstetric Diseases; Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology; The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China. cbslhy@163.com.
Lanxiang ZhuDepartment of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou, China. zhulanxiang0125@163.com.
Mingsong LiDepartment of Gastroenterology; Guangdong Provincial Key Laboratory of Major Obstetric Diseases; Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology; The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China. lims661216@163.com.ORCID http://orcid.org/0000-0003-2115-5928

Funding

Guangdong Medical Research Foundation (Guangdong Province Medical Research Foundation) 2022A1515111193Guangzhou Science and Technology Program key projects 2023A04J0581Guangzhou Science and Technology Program key projects 2024B03J0466National Natural Science Foundation of China (National Science Foundation of China) 82303391National Natural Science Foundation of China (National Science Foundation of China) 82370529
6 · The paper itself

Abstract

backgroundThe pathogenesis of inflammatory bowel disease (IBD) involves chronic inflammation of the gastrointestinal tract, which predisposes patients to an increased risk of fibrosis and cancer due to prolonged inflammatory stimulation. However, the specific mechanisms underlying secondary gastrointestinal carcinogenesis in individuals with IBD remain poorly elucidated, particularly due to a limited number of studies conducted at single-nuclei level.

methodsWe investigated the dynamics and interactions of cell subtypes during the progression of IBD-associated cancers through comprehensive analysis including single-nuclei transcriptomics, spatial transcriptomics, ecological dynamic modelling, multiplex immunohistochemistry, in vitro co-culture and in vivo animal studies.

resultsThe results revealed that CXCL14+ fibroblasts, the primary source of collagen in the microenvironment, play a pivotal role in the inflammation-cancer transition. These fibroblasts progressively increase in abundance during this transition and secreted elevated levels of collagen IV. The increased presence of collagen IV promotes the recruitment and differentiation of SPP1+ macrophages. This interaction ultimately contributes to the development and progression of IBD-associated fibrosis and cancer transformation. Collagen IV, secreted by CXCL14+ fibroblasts, plays a pivotal role in promoting the transition from IBD to cancer. Inhibition of collagen IV secretion not only prevents fibrosis but also hinders the development of inflammation-cancer transition.

conclusionOur findings are crucial for understanding the mechanisms underlying IBD-associated cancer and developing innovative therapeutic strategies. During the inflammation-cancer transition, activation of the SOX4 leads to increased COL4A1/A2 secretion by CXCL14+ fibroblasts, resulting in enhanced collagen IV synthesis. Collagen IV binds to ITGB1/CD44 receptors on SPP1+ macrophages and activates EGR1/2 to promote SPP1+ macrophage differentiation, while upregulating S100A10 and ANXA2. Activation of S100A10 and ANXA2 promotes recruitment of SPP1+ macrophages, which contributes to immune escape and secretion of oncogenes, thus further promoting fibrosis and tumorigenesis. In addition, SPP1+ macrophages further stimulate CXCL14+ fibroblasts to secrete COL4A1/A2 via TGF-β1, forming a feedback loop that amplifies interactions in the tumour microenvironment.

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PMID42892644

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