ArticleOncology letters2021
Cancer-associated fibroblast-secreted collagen triple helix repeat containing-1 promotes breast cancer cell migration, invasiveness and epithelial-mesenchymal transition by activating the Wnt/β-catenin pathway.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 26 citations in OpenAlex.
- Integrated scRNA-Seq and Spatial Transcriptomics Reveal CHPF and GPC1 as Markers of Cancer-Associated Fibroblast-Dominant Domains in Colorectal Cancer.Cancer medicine · 2026Article
- The Roles of MicroRNAs, Oncogenes, and Tumor Suppressor Gene Molecular Subtypes of Breast Cancer: Therapeutic Potential of Pharmaceutical and Natural Products.International journal of breast cancer · 2026Review
- Cancer‑associated fibroblasts in human malignancies, with a particular emphasis on sarcomas (Review).International journal of oncology · 2025Review
- Emerging Concepts in Fibroblast Biology and Progressive Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- Transforming Cancer Therapy: Unlocking the Potential of Targeting Vascular and Stromal Cells in the Tumor Microenvironment.Cancer research · 2025Review
- Nano-drug delivery strategies affecting cancer-associated fibroblasts to reduce tumor metastasis.Acta pharmaceutica Sinica. B · 2025Review
- Review
- Pan-cancer drivers of metastasis.Molecular cancer · 2025Article
- CTHRC1: a key player in colorectal cancer progression and immune evasion.Frontiers in immunology · 2025Review
- The role of CAFs in therapeutic resistance in triple negative breast cancer: an emerging challenge.Frontiers in molecular biosciences · 2025Review
- The Biological Roles and Clinical Applications of the PI3K/AKT Pathway in Targeted Therapy Resistance in HER2-Positive Breast Cancer: A Comprehensive Review.International journal of molecular sciences · 2024Review
- CTHRC1Scientific reports · 2024Article
- Systematic dissection of tumor-normal single-cell ecosystems across a thousand tumors of 30 cancer types.Nature communications · 2024Article
- The role of collagen triple helix repeat containing 1 (CTHRC1) in cancer development and progression.Expert opinion on therapeutic targets · 2024Review
- Exploring the interaction between extracellular matrix components in a 3D organoid disease model to replicate the pathophysiology of breast cancer.Journal of experimental & clinical cancer research : CR · 2023Review
- CTHRC1, a novel gene with multiple functions in physiology, disease and solid tumors (Review).Oncology letters · 2023Review
- Fibroblasts as Turned Agents in Cancer Progression.Cancers · 2023Review
- An integrated single-cell transcriptomic dataset for non-small cell lung cancer.Scientific data · 2023Article
- SARA suppresses myofibroblast precursor transdifferentiation in fibrogenesis in a mouse model of scleroderma.JCI insight · 2022Article
- Application of collagen triple helix repeat containing-1 and mitotic spindle apparatus antibody in small cell lung cancer diagnosis.Journal of clinical laboratory analysis · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer-associated fibroblasts (CAFs) are continuously activated and are one of the most important cellular components of the tumor matrix. The role of CAFs in the tumor microenvironment has been widely recognized. However, the underlying molecular mechanism by which CAFs promote tumor characteristics in breast cancer (BC) remains poorly understood. The aim of the present study was to investigate the potential mechanisms and the possible pathways of collagen triple helix repeat containing-1 (CTHRC1) in the epithelial-mesenchymal transition (EMT) of BC cells. The level of CTHRC1 in BC tissues was found to be higher than that in adjacent-normal tissues. CAFs isolated from BC tissues secreted significantly greater amounts of CTHRC1 than normal fibroblasts. Furthermore, CAFs promoted the migration, invasiveness and EMT of BC cells by secreting CTHRC1, which activates the Wnt/β-catenin signaling pathway. However, the use of neutralizing antibodies towards CTHRC1, or the specific inhibitor Dickkopf-1, to inhibit the Wnt/β catenin pathway significantly alleviated the CAF-induced malignant phenotypes of BC cells. Collectively, the data indicate that CAFs in the tumor microenvironment promote BC cell malignant behaviors via the CTHRC1/Wnt/β-catenin signaling pathway. Furthermore, weakening CAF-BC cell communication by suppressing CTHRC1 expression may be a novel strategy for treating BC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.