---
title: "CXCL14+ fibroblasts drive IBD-associated fibrosis and cancer through collagen IV–SPP1+ macrophage"
id: "british-journal-of-cancer-0-cxcl14-fibroblasts-promote-development-of-ibd-associated-fibrosis-and-cancer-by"
canonical_url: "https://medichelpline.com/clinical-feed/british-journal-of-cancer-0-cxcl14-fibroblasts-promote-development-of-ibd-associated-fibrosis-and-cancer-by"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "British Journal of Cancer"
source_url: "https://www.nature.com/articles/s41416-026-03636-2"
published_at: "2026-10-17T12:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# CXCL14+ fibroblasts drive IBD-associated fibrosis and cancer through collagen IV–SPP1+ macrophage
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/british-journal-of-cancer-0-cxcl14-fibroblasts-promote-development-of-ibd-associated-fibrosis-and-cancer-by
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** British Journal of Cancer
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41416-026-03636-2)
- **Published At:** 2026-10-17T12:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- Investigators used single-nuclei transcriptomics, spatial transcriptomics, ecological dynamic modelling, multiplex immunohistochemistry, in vitro co-culture and in vivo animal studies to map cellular interactions during IBD-associated tumourigenesis. - The study team observed progressive expansion of a **CXCL14+ fibroblast** population during the inflammation-to-cancer transition in IBD tissues. - Data indicated that these fibroblasts are the dominant local source of extracellular matrix and secrete elevated levels of **collagen IV** (COL4A1/A2). - Collagen IV was reported to recruit and drive differentiation of **SPP1+ macrophages** via binding to **ITGB1/CD44** receptors and activation of EGR1/EGR2 transcriptional programs. - Authors noted that SPP1+ macrophages upregulate S100A10 and ANXA2, which the cohort linked to macrophage recruitment and oncogenic secretory activity. - The study team described a reciprocal loop: SPP1+ macrophages stimulate CXCL14+ fibroblasts through TGF-β1 to increase COL4A1/A2 secretion, amplifying fibrosis and tumour-promoting interactions. - In vivo experiments, as summarized in the source, showed that CXCL14 and collagen IV promote colitis-associated tumourigenesis; treatment with a DDR1/2 inhibitor restrained tumour formation in the reported model. - Figures presented include single-nuclei sequencing maps, cell-type frequency changes, spatial co-localisation, mechanistic pathway schematics, and pharmacologic intervention data. - The authors deposited raw sequencing data in the Genome Sequence Archive (GSA-Human: HRA009030) and analysed public datasets from GDC and GEO; they stated raw data are available on request and code can be obtained by contacting the authors. - The paper did not provide patient-level demographic breakdowns or detailed dosing regimens for pharmacologic inhibition in the abstract; specific methodology and numerical metrics are contained within the full article.
## Clinical Analysis & Structured Key Points
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[articles](https://www.nature.com/bjc/articles?type=article) 4. article * Article * Published: 17 October 2026 Cellular and Molecular Biology # CXCL14+ fibroblasts promote development of IBD-associated fibrosis and cancer by interacting with SPP1+ macrophages via collagen IV secretion * [Haonan Zhang](https://www.nature.com/articles/s41416-026-03636-2#auth-Haonan-Zhang-Aff1)[1](https://www.nature.com/articles/s41416-026-03636-2#Aff1) [na1](https://www.nature.com/articles/s41416-026-03636-2#na1), * [Yulu Shi](https://www.nature.com/articles/s41416-026-03636-2#auth-Yulu-Shi-Aff2)[2](https://www.nature.com/articles/s41416-026-03636-2#Aff2) [na1](https://www.nature.com/articles/s41416-026-03636-2#na1), * [Qiuyu Song](https://www.nature.com/articles/s41416-026-03636-2#auth-Qiuyu-Song-Aff1)[1](https://www.nature.com/articles/s41416-026-03636-2#Aff1) [na1](https://www.nature.com/articles/s41416-026-03636-2#na1), * [Na Li](https://www.nature.com/articles/s41416-026-03636-2#auth-Na-Li-Aff3)[3](https://www.nature.com/articles/s41416-026-03636-2#Aff3), * [Zhaoxian Lin](https://www.nature.com/articles/s41416-026-03636-2#auth-Zhaoxian-Lin-Aff1)[1](https://www.nature.com/articles/s41416-026-03636-2#Aff1), * [Qiusan Chen](https://www.nature.com/articles/s41416-026-03636-2#auth-Qiusan-Chen-Aff1)[1](https://www.nature.com/articles/s41416-026-03636-2#Aff1), * [Yi Yang](https://www.nature.com/articles/s41416-026-03636-2#auth-Yi-Yang-Aff1)[1](https://www.nature.com/articles/s41416-026-03636-2#Aff1), * [Yanjun Chen](https://www.nature.com/articles/s41416-026-03636-2#auth-Yanjun-Chen-Aff4)[4](https://www.nature.com/articles/s41416-026-03636-2#Aff4), * [Qian Liu](https://www.nature.com/articles/s41416-026-03636-2#auth-Qian-Liu-Aff5)[5](https://www.nature.com/articles/s41416-026-03636-2#Aff5), * [Yan Tan](https://www.nature.com/articles/s41416-026-03636-2#auth-Yan-Tan-Aff6)[6](https://www.nature.com/articles/s41416-026-03636-2#Aff6), * [Yifeng Zheng](https://www.nature.com/articles/s41416-026-03636-2#auth-Yifeng-Zheng-Aff1)[1](https://www.nature.com/articles/s41416-026-03636-2#Aff1), * [Shanping Wang](https://www.nature.com/articles/s41416-026-03636-2#auth-Shanping-Wang-Aff1)[1](https://www.nature.com/articles/s41416-026-03636-2#Aff1), * [Yan Sun](https://www.nature.com/articles/s41416-026-03636-2#auth-Yan-Sun-Aff1)[1](https://www.nature.com/articles/s41416-026-03636-2#Aff1), * [Xiaxi Li](https://www.nature.com/articles/s41416-026-03636-2#auth-Xiaxi-Li-Aff7)[7](https://www.nature.com/articles/s41416-026-03636-2#Aff7), * [Chengcheng He](https://www.nature.com/articles/s41416-026-03636-2#auth-Chengcheng-He-Aff1)[1](https://www.nature.com/articles/s41416-026-03636-2#Aff1), * [Lanxiang Zhu](https://www.nature.com/articles/s41416-026-03636-2#auth-Lanxiang-Zhu-Aff4)[4](https://www.nature.com/articles/s41416-026-03636-2#Aff4) & * … * [Mingsong Li](https://www.nature.com/articles/s41416-026-03636-2#auth-Mingsong-Li-Aff1-Aff8) [ORCID: orcid.org/0000-0003-2115-5928](https://orcid.org/0000-0003-2115-5928)[1](https://www.nature.com/articles/s41416-026-03636-2#Aff1),[8](https://www.nature.com/articles/s41416-026-03636-2#Aff8) Show authors [_British Journal of Cancer_](https://www.nature.com/bjc) (2026) [Cite this article](https://www.nature.com/articles/s41416-026-03636-2#citeas) Save article [ View saved research ](https://www.nature.com/saved-research) ## Abstract ### Background The 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. ### Methods We 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. ### Results The 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. ### Conclusion Our findings are crucial for understanding the mechanisms underlying IBD-associated cancer and developing innovative therapeutic strategies. ![](https://media.springernature.com/lw685/springer-static/image/art%3A10.1038%2Fs41416-026-03636-2/MediaObjects/41416_2026_3636_Figa_HTML.png) 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. This is a preview of subscription content, [access via your institution](https://wayf.springernature.com?redirect_uri=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41416-026-03636-2) ## Access options [ Access through your institution ](https://wayf.springernature.com?redirect_uri=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41416-026-03636-2) Subscribe to this journal Receive 24 print issues and online access 251,40 € per year only 10,48 € per issue [Learn more](https://www.nature.com/bjc/subscribe) Buy this article * Purchase on SpringerLink * Instant access to the full article PDF. 39,95 € Prices may be subject to local taxes which are calculated during checkout ### Additional access options: * [Log in](https://idp.nature.com/auth/personal/springernature?client_id=grover&redirect_uri=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41416-026-03636-2) * [Learn about institutional subscriptions](https://www.springernature.com/gp/librarians/licensing/license-options) * [Read our FAQs](https://support.nature.com/en/support/home) * [Contact customer support](https://www.springernature.com/gp/contact) **Fig. 1: Single-nuclei sequencing of IBD-related cancer development.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03636-2/MediaObjects/41416_2026_3636_Fig1_HTML.png) **Fig. 2: CXCL14+ fibroblasts are associated with IBD-related cancer progression.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03636-2/MediaObjects/41416_2026_3636_Fig2_HTML.png) **Fig. 3: CXCL9+/ SPP1+ macrophages ratio decreases during IBD-related cancer progression.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03636-2/MediaObjects/41416_2026_3636_Fig3_HTML.png) **Fig. 4: CXCL14+ fibroblasts are positively correlated with SPP1+ macrophage infiltration and interact with SPP1+ macrophages by secreting collagen IV in IBD-associated cancer.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03636-2/MediaObjects/41416_2026_3636_Fig4_HTML.png) **Fig. 5: The interactions between CXCL14+ fibroblasts and SPP1+ macrophages are more frequent in CMS4 of CRC.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03636-2/MediaObjects/41416_2026_3636_Fig5_HTML.png) **Fig. 6: CXCL14+ fibroblasts promote recruitment of SPP1+ macrophages by secreting collagen IV that binds to the ITGB1/CD44 receptor to activate EGR1/EGR2 to upregulate S100A10/ANXA2 expression.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03636-2/MediaObjects/41416_2026_3636_Fig6_HTML.png) **Fig. 7: CXCL14 and Collagen IV promote colitis-associated tumorigenesis in vivo.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03636-2/MediaObjects/41416_2026_3636_Fig7_HTML.png) **Fig. 8: Treatment with DDR1/2 inhibitor can restrain the colitis-associated tumorigenesis.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03636-2/MediaObjects/41416_2026_3636_Fig8_HTML.png) ### Explore related subjects Discover the latest articles and news in related subjects. * [Autoimmunity](https://www.nature.com/subjects/autoimmunity) * [Cancer microenvironment](https://www.nature.com/subjects/cancer-microenvironment) ## Data availability All of the raw data could be made available upon request. The raw sequence data reported in this paper have been deposited in the Genome Sequence Archive in National Genomics Data Center, China National Center for Bioinformation/Beijing Institute of Genomics, Chinese Academy of Sciences (GSA-Human: HRA009030) that are publicly accessible at [[58](https://www.nature.com/articles/s41416-026-03636-2#ref-CR58 "Chen T, Chen X, Zhang S, Zhu J, Tang B, Wang A, et al. The Genome Sequence Archive Family: Toward Explosive Data Growth and Diverse Data Types. Genomics Proteom Bioinforma. 2021;19:578–83."), [59](https://www.nature.com/articles/s41416-026-03636-2#ref-CR59 "Database Resources of the National Genomics Data Center, China National Center for Bioinformation in 2022. Nucleic Acids Res. 2022; 50: D27-D38.")]. Publicly available datasets were analysed in this study. These data can be found here: and . ## Code availability All code are available by contacting the authors. ## References 1. Faye AS, Holmer AK, Axelrad JE. 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