ArticleThe American journal of pathology2008
Mammary epithelial-specific disruption of focal adhesion kinase retards tumor formation and metastasis in a transgenic mouse model of human breast cancer.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
What it found
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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.
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Who cites it
90 citing papers in PubMed, 134 citations in OpenAlex.
- Endothelial Cell pY397-FAK Expression Predicts the Risk of Breast Cancer Recurrences after Radiotherapy in the SweBCG91-RT Cohort.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Trial
- Low-dose tamoxifen treatment reduces collagen organisation indicative of tissue stiffness in the normal breast: results from the KARISMA randomised controlled trial.Breast cancer research : BCR · 2024Trial
- A highly potent bi-thiazole inhibitor of LOX rewires collagen architecture and enhances chemoresponse in triple-negative breast cancer.Cell chemical biology · 2024Article
- Emerin mislocalization during chromatin bridge resolution can drive prostate cancer cell invasiveness in a collagen-rich microenvironment.Experimental & molecular medicine · 2024Article
- Cancer as a biophysical disease: Targeting the mechanical-adaptability program.Biophysical journal · 2022Review
- BHMPS Inhibits Breast Cancer Migration and Invasion by Disrupting Rab27a-Mediated EGFR and Fibronectin Secretion.Cancers · 2022Article
- Review
- The Dynamic Interaction between Extracellular Matrix Remodeling and Breast Tumor Progression.Cells · 2021Review
- Review
- ARHGEF3 Associated with Invasion, Metastasis, and Proliferation in Human Osteosarcoma.BioMed research international · 2021Article
- Photocleavable Surfactant-Enabled Extracellular Matrix Proteomics.Analytical chemistry · 2020Article
- Collagen-rich omentum is a premetastatic niche for integrin α2-mediated peritoneal metastasis.eLife · 2020Article
- FAK activates AKT-mTOR signaling to promote the growth and progression of MMTV-Wnt1-driven basal-like mammary tumors.Breast cancer research : BCR · 2020Article
- Article
- Development of a Fragment-Based Screening Assay for the Focal Adhesion Targeting Domain Using SPR and NMR.Molecules (Basel, Switzerland) · 2019Article
- Increased Expression of MicroRNA 551a by c-Fos Reduces Focal Adhesion Kinase Levels and Blocks Tumorigenesis.Molecular and cellular biology · 2019Article
- Focal adhesion kinase (FAK) activation by estrogens involves GPER in triple-negative breast cancer cells.Journal of experimental & clinical cancer research : CR · 2019Article
- Cancer cells' ability to mechanically adjust to extracellular matrix stiffness correlates with their invasive potential.Molecular biology of the cell · 2018Article
- Modeling Tissue Polarity in Context.Journal of molecular biology · 2018Review
- Hippo component YAP promotes focal adhesion and tumour aggressiveness via transcriptionally activating THBS1/FAK signalling in breast cancer.Journal of experimental & clinical cancer research : CR · 2018Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Focal adhesion kinase (FAK) is a central regulator of the focal adhesion, influencing cell proliferation, survival, and migration. Despite evidence demonstrating FAK overexpression in human cancer, its role in tumor initiation and progression is not well understood. Using Cre/LoxP technology to specifically knockout FAK in the mammary epithelium, we showed that FAK is not required for tumor initiation but is required for tumor progression. The mechanistic underpinnings of these results suggested that FAK regulates clinically relevant gene signatures and multiple signaling complexes associated with tumor progression and metastasis, such as Src, ERK, and p130Cas. Furthermore, a systems-level analysis identified FAK as a major regulator of the tumor transcriptome, influencing genes associated with adhesion and growth factor signaling pathways, and their cross talk. Additionally, FAK was shown to down-regulate the expression of clinically relevant proliferation- and metastasis-associated gene signatures, as well as an enriched group of genes associated with the G(2) and G(2)/M phases of the cell cycle. Computational analysis of transcription factor-binding sites within ontology-enriched or clustered gene sets suggested that the differentially expressed proliferation- and metastasis-associated genes in FAK-null cells were regulated through a common set of transcription factors, including p53. Therefore, FAK acts as a primary node in the activated signaling network in transformed motile cells and is a prime candidate for novel therapeutic interventions to treat aggressive human breast cancers.
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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.