ArticleOncogene2008
Identification of VEGF-regulated genes associated with increased lung metastatic potential: functional involvement of tenascin-C in tumor growth and lung metastasis.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 79 citations in OpenAlex.
- Estrogen plus progestin and breast cancer incidence and mortality in postmenopausal women.JAMA · 2010Trial
- Oestrogen plus progestin and lung cancer in postmenopausal women (Women's Health Initiative trial): a post-hoc analysis of a randomised controlled trial.Lancet (London, England) · 2009Trial
- Review
- Investigating Chemokine-Matrix Networks in Breast Cancer: Tenascin-C Sets the Tone for CCL2.International journal of molecular sciences · 2023Article
- The covert symphony: cellular and molecular accomplices in breast cancer metastasis.Frontiers in cell and developmental biology · 2023Review
- Tenascin-C: A Key Regulator in Angiogenesis during Wound Healing.Biomolecules · 2022Review
- Thorny ground, rocky soil: Tissue-specific mechanisms of tumor dormancy and relapse.Seminars in cancer biology · 2022Review
- The genomic architecture of metastasis in breast cancer: focus on mechanistic aspects, signalling pathways and therapeutic strategies.Medical oncology (Northwood, London, England) · 2021Review
- Assessment of the WAP-Myc mouse mammary tumor model for spontaneous metastasis.Scientific reports · 2020Article
- Periostin and tenascin-C interaction promotes angiogenesis in ischemic proliferative retinopathy.Scientific reports · 2020Article
- Article
- Cell Intrinsic and Extrinsic Mechanisms of Caveolin-1-Enhanced Metastasis.Biomolecules · 2019Review
- Lung-Seeking Metastases.Cancers · 2019Review
- Tenascin-C expression contributes to pediatric brainstem glioma tumor phenotype and represents a novel biomarker of disease.Acta neuropathologica communications · 2019Article
- Molecular Mechanisms of Breast Cancer Metastasis to the Lung: Clinical and Experimental Perspectives.International journal of molecular sciences · 2019Review
- Significance of Intratumoral Fibrosis in Clear Cell Renal Cell Carcinoma.Journal of pathology and translational medicine · 2018Article
- Targeted matrisome analysis identifies thrombospondin-2 and tenascin-C in aligned collagen stroma from invasive breast carcinoma.Scientific reports · 2018Article
- WT1 expression in breast cancer disrupts the epithelial/mesenchymal balance of tumour cells and correlates with the metabolic response to docetaxel.Scientific reports · 2017Article
- Tenascin-C secreted by transdifferentiated retinal pigment epithelial cells promotes choroidal neovascularization via integrin αV.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- EMT reversal in human cancer cells after IR knockdown in hyperinsulinemic mice.Endocrine-related cancer · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Metastasis is the primary cause of death in patients with breast cancer. Overexpression of c-myc in humans correlates with metastases, but transgenic mice only show low rates of micrometastases. We have generated transgenic mice that overexpress both c-myc and vascular endothelial growth factor (VEGF) (Myc/VEGF) in the mammary gland, which develop high rates of pulmonary macrometastases. Gene expression profiling revealed a set of deregulated genes in Myc/VEGF tumors compared to Myc tumors associated with the increased metastatic phenotype. Cross-comparisons between this set of genes with a human breast cancer lung metastasis gene signature identified five common targets: tenascin-C(TNC), matrix metalloprotease-2, collagen-6-A1, mannosidase-alpha-1A and HLA-DPA1. Signaling blockade or knockdown of TNC in MDA-MB-435 cells resulted in a significant impairment of cell migration and anchorage-independent cell proliferation. Mice injected with clonal MDA-MB-435 cells with reduced expression of TNC demonstrated a significant decrease (P<0.05) in (1) primary tumor growth; (2) tumor relapse after surgical removal of the primary tumor and (3) incidence of lung metastasis. Our results demonstrate that VEGF induces complex alterations in tissue architecture and gene expression. The TNC signaling pathway plays an important role in mammary tumor growth and metastases, suggesting that TNC may be a relevant target for therapy against metastatic breast cancer.
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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.