ReviewCell cycle (Georgetown, Tex.)2008
FERM control of FAK function: implications for cancer therapy.
Review in Cell cycle (Georgetown, Tex.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 136 citations in OpenAlex.
- Randomized, Open-Label, Crossover Studies Evaluating the Effect of Food and Liquid Formulation on the Pharmacokinetics of the Novel Focal Adhesion Kinase (FAK) Inhibitor BI 853520.Targeted oncology · 2019Trial
- Loss of endothelial cell FAK represses cisplatin-induced vascular senescence in distal niches to reduce lung metastatic burden.Research square · 2026Article
- Mechanisms Involved in Focal Adhesion Signaling Regulating Tumor Anoikis Resistance.Cancer science · 2025Review
- Focal adhesion kinase: A promising regulator of colitis-associated healing.World journal of gastroenterology · 2025Review
- Adipocyte-derived CXCL10 in obesity promotes the migration and invasion of ovarian cancer cells.Journal of ovarian research · 2024Article
- Low concentrations of saracatinib promote definitive endoderm differentiation through inhibition of FAK-YAP signaling axis.Cell communication and signaling : CCS · 2024Article
- Acinar to β-like cell conversion through inhibition of focal adhesion kinase.Nature communications · 2024Article
- Blood-testis barrier: a review on regulators in maintaining cell junction integrity between Sertoli cells.Cell and tissue research · 2024Review
- Vinorelbine Improves the Efficacy of Sorafenib against Hepatocellular Carcinoma: A Promising Therapeutic Approach.International journal of molecular sciences · 2024Article
- Focal adhesion kinase-mediated signaling controls the onset of pancreatic cell differentiation.Development (Cambridge, England) · 2022Article
- Phosphorylation of Focal Adhesion Kinase at Y925: Role in Glia-Dependent and Independent Migration through Regulating Cofilin and N-Cadherin.Molecular neurobiology · 2022Article
- Manipulation of Focal Adhesion Signaling by Pathogenic Microbes.International journal of molecular sciences · 2021Review
- Involvement of the FAK Network in Pathologies Related to Altered Mechanotransduction.International journal of molecular sciences · 2020Review
- Identification of new binding proteins of focal adhesion kinase using immunoprecipitation and mass spectrometry.Scientific reports · 2019Article
- The roles of nuclear focal adhesion kinase (FAK) on Cancer: a focused review.Journal of experimental & clinical cancer research : CR · 2019Review
- Phase I Study of the Focal Adhesion Kinase Inhibitor BI 853520 in Japanese and Taiwanese Patients with Advanced or Metastatic Solid Tumors.Targeted oncology · 2019Article
- Inhibiting focal adhesion kinase: A potential target for enhancing therapeutic efficacy in colorectal cancer therapy.World journal of gastrointestinal oncology · 2018Article
- Endogenous Control Mechanisms of FAK and PYK2 and Their Relevance to Cancer Development.Cancers · 2018Review
- Inhibition of cell migration by focal adhesion kinase: Time-dependent difference in integrin-induced signaling between endothelial and hepatoblastoma cells.International journal of molecular medicine · 2018Article
- FAK auto-phosphorylation site tyrosine 397 is required for development but dispensable for normal skin homeostasis.PloS one · 2018Article
10 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Integrins are transmembrane receptors that bind to extracellular matrix proteins and convey anchorage-dependent signals regulating normal cell proliferation. Integrin signals within the tumor micro-environment also impact cancer cell survival and invasion during tumor progression. These integrin-associated signaling events are transduced in part through the activation of non-receptor protein-tyrosine kinases. Focal adhesion kinase (FAK) is activated by beta-subunit integrins in both normal and transformed cells. As genetic inactivation of beta1 integrin or FAK yield early embryonic lethal phenotypes associated with decreased cell proliferation, and dominant-negative inhibition of FAK can cause increased cell apoptosis, there is a concern that FAK inhibition may have cytotoxic effects on cell growth or survival. However, FAK-specific small molecule inhibitors do not directly impact cell growth in culture, but yet show potent anti-tumor growth effects in vivo. Additionally, recent studies have shed new insight into the FAK kinase-independent regulation of cell proliferation and survival mediated by the FAK N-terminal FERM (band 4.1, ezrin, radixin, moesin homology) domain. Herein, we review the role of the FAK FERM domain in both the intrinsic regulation of FAK kinase activity and how FERM-mediated nuclear localization of FAK promotes enhanced cell survival through the inhibition of tumor suppressor p53 activation during development and under conditions of cellular stress. As we find that FAK FERM-mediated regulation of p53 occurs in human carcinoma cells, elevated FAK expression in tumors may promote both kinase-dependent and -independent survival mechanisms. We discuss how the pharmacological inhibition of FAK kinase activity may impact tumor progression through combined effects of blocking both tumor- and stromal-associated signaling regulating neo-vascularization.
Indexed as
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What OpenQuestion holds
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.