ArticleBritish journal of cancer2019
MicroRNA-222 reprogrammed cancer-associated fibroblasts enhance growth and metastasis of breast cancer.
Article in British journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 59 citations in OpenAlex.
- Cancer-associated fibroblasts: The silent conductors of tumor evolution and therapy refractoriness.Molecular biology reports · 2026Review
- Emerging role of microRNAs as modulators of the tumor immune microenvironment.Journal for immunotherapy of cancer · 2026Review
- Histology-defined activated cancer-associated fibroblasts are associated with poor survival in diffuse-type gastric adenocarcinoma.Virchows Archiv : an international journal of pathology · 2026Article
- Bioinformatics Analysis of microRNAs Associated with Metastatic Potential in Breast Cancer.Biology · 2026Article
- Melanoma and its fibroblastic allies: the emerging importance of CAFs in immune suppression, ECM modulation, and therapy resistance.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- The role of MiRNA-mediated tumor microenvironment in bone metastasis from a multi-omics perspective: cross-cancer mechanisms and clinical translation.Frontiers in oncology · 2026Review
- Cancer‑associated fibroblasts in human malignancies, with a particular emphasis on sarcomas (Review).International journal of oncology · 2025Review
- Integrative Bioinformatic Analysis of Cellular Senescence Genes in Ovarian Cancer: Molecular Subtyping, Prognostic Risk Stratification, and Chemoresistance Prediction.Biomedicines · 2025Article
- Potential biological roles of exosomal non-coding RNAs in breast cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Noncoding RNAs, Vital Players in Breast Cancer Metastasis.Breast cancer (Dove Medical Press) · 2025Review
- Mechanism insights and therapeutic intervention of tumor metastasis: latest developments and perspectives.Signal transduction and targeted therapy · 2024Review
- Advances in targeting cancer-associated fibroblasts through single-cell spatial transcriptomic sequencing.Biomarker research · 2024Review
- Extracellular Vesicles in Infrapatellar Fat Pad from Osteoarthritis Patients Impair Cartilage Metabolism and Induce Senescence.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Crosstalk and plasticity driving between cancer-associated fibroblasts and tumor microenvironment: significance of breast cancer metastasis.Journal of translational medicine · 2023Review
- MicroRNAs mediated interaction of tumor microenvironment cells with breast cancer cells during bone metastasis.Breast cancer (Tokyo, Japan) · 2023Review
- Integrating single-cell and bulk RNA sequencing to predict prognosis and immunotherapy response in prostate cancer.Scientific reports · 2023Article
- Non-Coding RNAs: Foes or Friends for Targeting Tumor Microenvironment.Non-coding RNA · 2023Review
- Fibroblasts as Turned Agents in Cancer Progression.Cancers · 2023Review
- Circulating exosomal microRNAs as potential prognostic biomarkers in gastrointestinal cancers: a systematic review and meta-analysis.Cancer cell international · 2023Review
- Fibroblast heterogeneity: Keystone of tissue homeostasis and pathology in inflammation and ageing.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundCancer-associated fibroblasts (CAFs) are known to impact on tumour behaviour, but the mechanisms controlling this are poorly understood.
methodsBreast normal fibroblasts (NFs) or CAFs were isolated from cancers by laser microdissection or were cultured. Fibroblasts were transfected to manipulate miR-222 or Lamin B receptor (LBR). The fibroblast-conditioned medium was collected and used to treat epithelial BC lines MDA-MB-231 and MDA-MB-157. Migration, invasion, proliferation or senescence was assessed using transwell, MTT or X-gal assays, respectively.
resultsMiR-222 was upregulated in CAFs as compared with NFs. Ectopic miR-222 expression in NFs induced CAF-like expression profiles, while miR-222 knockdown in CAFs inhibited CAF phenotypes. LBR was identified as a direct miR-222 target, and was functionally relevant since LBR knockdown phenocopied miR-222 overexpression and LBR overexpression phenocopied miR-222 knockdown. MiR-222 overexpression, or LBR knockdown, was sufficient to induce NFs to show the CAF characteristics of enhanced migration, invasion and senescence, and furthermore, the conditioned medium from these fibroblasts induced increased BC cell migration and invasion. The reverse manipulations in CAFs inhibited these behaviours in fibroblasts, and inhibited paracrine influences on BC cells.
conclusionMiR-222/LBR have key roles in controlling pro-progression influences of CAFs in BC. This pathway may present therapeutic opportunities to inhibit CAF-induced cancer progression.
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