ArticleOncogene2021
CTGF regulates cell proliferation, migration, and glucose metabolism through activation of FAK signaling in triple-negative breast cancer.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 69 citations in OpenAlex.
- Lysosome-directed targeted protein degradation technologies for overcoming cancer drug resistance: mechanisms, design principles, and therapeutic opportunities.Drug delivery · 2026Review
- CTGF: The remodeler of the tumor immune microenvironment (Review).Oncology reports · 2026Review
- SDC1Gut · 2026Article
- Menaquinone-7 alleviates mitochondrial dysfunction and senescence in senile osteoporosis by targeting the PINK1-mediated mitophagy via PXR/ERK/CREB signaling pathway.Journal of pharmaceutical analysis · 2026Article
- Biomimetic nanodecoys remodel the mechano-immune microenvironment to potentiate checkpoint blockade in colorectal cancer.Journal of nanobiotechnology · 2026Article
- Expanding the Spectrum of Src-Family Kinase-Related Autoinflammatory Diseases: Monogenic Vasculitis Caused By Germline Pathogenic Variants in HCK and FGR.Journal of clinical immunology · 2026Article
- Connective tissue growth factor contributes to resistance to anti-angiogenic therapies in renal cancer.Theranostics · 2026Article
- Myokines in cancer: bridging molecular mechanisms to biomarker discovery and therapeutic innovation.Frontiers in oncology · 2026Review
- CTGF knockdown in Vero cells reduces autophagy and adhesion and promotes short-term suspension adaptation.Frontiers in bioengineering and biotechnology · 2026Article
- The Hippo Pathway in Metaplastic Breast Carcinoma: Prognostic Significance and Therapeutic Implications.Current issues in molecular biology · 2025Article
- Targeting CTGF overcomes resistance to CSF1R inhibitors by preventing CAF activation in colorectal cancer.Cell reports. Medicine · 2025Article
- Downregulated of CTGF reveals mechanism, remodels immune microenvironment, modulates drug sensitivity in bladder cancer.Future science OA · 2025Article
- Integrin αvβ3 as a Non-Genomic Estrogen Receptor in Breast Cancer for Signaling Pathways and Crosstalk.Cells · 2025Review
- The Glyco-Switch of life: O-GlcNAcylation in cell fate decision.Glycobiology · 2025Review
- Multi-Target Therapeutic Potential of Arctii Fructus Lignans in Diabetes Mellitus and Its Complications: A Mechanistic Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Piezo1/ITGB1 Synergizes With CaCancer medicine · 2025Article
- Anti-CTGF/PD-1 bispecific antibody Y126S restrains desmoplastic and immunosuppressive microenvironment in pancreatic cancer.Journal for immunotherapy of cancer · 2025Article
- A Self-Assembling LYTAC Mediates CTGF Degradation and Remodels Inflammatory Tumor Microenvironment for Triple-Negative Breast Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mechanisms of breast cancer metastasis: the role of extracellular matrix.Molecular and cellular biochemistry · 2025Review
- Research progress on ADAM28 in malignant tumors.Discover oncology · 2025Review
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
Connective tissue growth factor (CTGF), also known as CCN2, is a member of the CCN protein family of secreted proteins with roles in diverse biological processes. CTGF regulates biological functions such as cell proliferation, migration, adhesion, wound healing, and angiogenesis. In this study, we demonstrate a mechanistic link between CTGF and enhanced aerobic glycolysis in triple-negative breast cancer (TNBC). We found that CTGF is overexpressed in TNBC and high CTGF expression is correlated with a poor prognosis. Also, CTGF was required for in vivo tumorigenesis and in vitro proliferation, migration, invasion, and adhesion of TNBC cells. Our results indicate that extracellular CTGF binds directly to integrin αvβ3, activating the FAK/Src/NF-κB p65 signaling axis, which results in transcriptional upregulation of Glut3. Neutralization of CTGF decreased cell proliferation, migration, and invasion through downregulation of Glut3-mediated glycolytic phenotypes. Overall, our work suggests a novel function for CTGF as a modulator of cancer metabolism, indicating that CTGF is a potential therapeutic target in TNBC.
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Registered trials
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.