ArticleJournal of experimental & clinical cancer research : CR2022
Tumor bud-derived CCL5 recruits fibroblasts and promotes colorectal cancer progression via CCR5-SLC25A24 signaling.
Article in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026Review
- CCL5 promotes colon cancer progression via PI3K/AKT signaling and is negatively regulated by STAT1.Journal of gastrointestinal oncology · 2026Article
- Identifying a cancer therapeutic target: Cell-SELEX identifies a membrane protein for aptamer-mediated growth suppression.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Comprehensive machine learning identifies anoikis signatures predicting therapeutic resistance and survival in gastric cancer.Scientific reports · 2026Article
- Article
- A full-automated tumor budding annotation approach in hematoxylin and eosin-stained whole slide images of colorectal cancer.NPJ precision oncology · 2025Article
- CCL5Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A new combined prognostic model involvingTranslational cancer research · 2025Article
- Comprehensive single-cell transcriptome landscape of metastatic colorectal cancer identifies budding-potential cells and their interactions with cancer-associated fibroblasts.NPJ precision oncology · 2025Article
- Deep learning-enabled multiphoton microscopy predicts colorectal cancer recurrence from routine FFPE specimens.NPJ digital medicine · 2025Article
- Endothelial cell in tumor angiogenesis: Origins, mechanisms, and therapeutic implication.Genes & diseases · 2025Review
- Tumor cell-derived osteopontin promotes tumor fibrosis indirectly via tumor-associated macrophages.Journal of translational medicine · 2025Article
- Redox disruption using electroactive liposome coated gold nanoparticles for cancer therapy.Nature communications · 2025Article
- Tumor cell-derived ISG15 promotes fibroblast recruitment in oral squamous cell carcinoma via CD11a-dependent glycolytic reprogramming.Oncogenesis · 2025Article
- SPP1hi macrophages, NKG7 T cells, CCL5hi fibroblasts, and IgM plasma cells are dominant features of necrobiosis.JCI insight · 2025Article
- Blockade of CCR5Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- CCL5/CCR5/CYP1A1 pathway prompts liver cancer cells to survive in the combination of targeted and immunological therapies.Cancer science · 2024Article
- Deciphering the impact of aggregated autophagy-related genes TUBA1B and HSP90AA1 on colorectal cancer evolution: a single-cell sequencing study of the tumor microenvironment.Discover oncology · 2024Article
- Advancements in 3D In Vitro Models for Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Programmed Cell Death-Related Gene Signature Associated with Prognosis and Immune Infiltration and the Roles of HMOX1 in the Proliferation and Apoptosis were Investigated in Uveal Melanoma.Genes & genomics · 2024Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundTumor budding is included in the routine diagnosis of colorectal cancer (CRC) and is considered a tumor prognostic factor independent of TNM staging. This study aimed to identify the fibroblast-mediated effect of tumor bud-derived C-C chemokine ligand 5 (CCL5) on the tumor microenvironment (TME).
methodsRecruitment assays and a human cytokine array were used to detect the main cytokines that CRC tumor buds secrete to recruit fibroblasts. siRNA transfection and inhibitor treatment were used to investigate the role of fibroblast CCL5 receptors in fibroblast recruitment. Subsequently, transcriptome sequencing was performed to explore the molecular changes occurring in fibroblasts upon stimulation with CCL5. Finally, clinical specimens and orthotopic xenograft mouse models were studied to explore the contribution of CCL5 to angiogenesis and collagen synthesis.
resultsHematoxylin-eosin staining and immunochemistry revealed a higher number of fibroblasts at the invasive front of CRC tissue showing tumor budding than at sites without tumor budding. In vitro experiments demonstrated that CCL5 derived from tumor buds could recruit fibroblasts by acting on the CCR5 receptors on fibroblasts. Tumor bud-derived CCL5 could also positively regulate solute carrier family 25 member 24 (SLC25A24) expression in fibroblasts, potentially activating pAkt-pmTOR signaling. Moreover, CCL5 could increase the number of α-SMA
conclusionsAt the invasive front of CRC, tumor bud-derived CCL5 can recruit fibroblasts via CCR5-SLC25A24 signaling, further promoting angiogenesis and collagen synthesis via recruited fibroblasts, and eventually create a tumor-promoting microenvironment. Therefore, CCL5 may serve as a potential diagnostic marker and therapeutic target for tumor budding in CRC.
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