ArticleTranslational oncology2009
Focal adhesion kinase functions as an akt downstream target in migration of colorectal cancer cells.
Article in Translational oncology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- TRIM72 inhibits cell migration and epithelial-mesenchymal transition by attenuating FAK/akt signaling in colorectal cancer.Heliyon · 2024Article
- Article
- EGFL6 promotes colorectal cancer cell growth and mobility and the anti-cancer property of anti-EGFL6 antibody.Cell & bioscience · 2021Article
- Article
- Repurposing of existing FDA approved drugs for Neprilysin inhibition: AnJournal of molecular structure · 2021Article
- Aerial Parts of Peucedanum chenur Have Anti-Cancer Properties through the Induction of Apoptosis and Inhibition of Invasion in Human Colorectal Cancer Cells.Iranian biomedical journal · 2020Article
- Multifaceted Roles of Caveolin-1 in Lung Cancer: A New Investigation Focused on Tumor Occurrence, Development and Therapy.Cancers · 2020Review
- The Psoriasis Therapeutic Potential of a Novel Short Laminin Peptide C16.International journal of molecular sciences · 2019Article
- Quantitative Proteomics Links the Intermediate Filament Nestin to Resistance to Targeted BRAF Inhibition in Melanoma Cells.Molecular & cellular proteomics : MCP · 2019Article
- ZINC4085554 inhibits cancer cell adhesion by interfering with the interaction of Akt1 and FAK.Oncology letters · 2019Article
- Regulation of focal adhesion turnover in SDF-1α-stimulated migration of mesenchymal stem cells in neural differentiation.Scientific reports · 2017Article
- A novel RON splice variant lacking exon 2 activates the PI3K/AKT pathway via PTEN phosphorylation in colorectal carcinoma cells.Oncotarget · 2017Article
- Neutral endopeptidase (NEP) is differentially involved in biological activities and cell signaling of colon cancer cell lines derived from various stages of tumor development.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- CCN1 (CYR61) and CCN3 (NOV) signaling drives human trophoblast cells into senescence and stimulates migration properties.Cell adhesion & migration · 2016Article
- Kaempferol-3-O-rutinoside from Afgekia mahidoliae promotes keratinocyte migration through FAK and Rac1 activation.Journal of natural medicines · 2015Article
- Hematopoietic cell kinase (HCK) as a therapeutic target in immune and cancer cells.Oncotarget · 2015Review
- Dendrofalconerol A sensitizes anoikis and inhibits migration in lung cancer cells.Journal of natural medicines · 2015Article
- Dentin phosphophoryn in the matrix activates AKT and mTOR signaling pathway to promote preodontoblast survival and differentiation.Frontiers in physiology · 2015Article
- FAK inhibition abrogates the malignant phenotype in aggressive pediatric renal tumors.Molecular cancer research : MCR · 2014Article
- PTEN regulates AMPA receptor-mediated cell viability in iPS-derived motor neurons.Cell death & disease · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Migration is a complex process that, besides its various physiological functions in embryogenesis and adult tissues, plays a crucial role in cancer cell invasion and metastasis. The focus of this study is the involvement and collaboration of Akt, focal adhesion kinase (FAK), and Src kinases in migration and invasiveness of colorectal cancer cells. We show that all three kinases can be found in one protein complex; nevertheless, the interaction between Akt and Src is indirect and mediated by FAK. Interestingly, induced Akt signaling causes an increase in tyrosine phosphorylation of FAK, but this increase is attenuated by the Src inhibitor SU6656. We also show that active Akt strongly stimulates cell migration, but this phenomenon is fully blocked by FAK knockdown or partly by inhibition of Src kinase. In addition, we found that all three kinases were indispensable for the successful invasion of colorectal cancer cells. Altogether, the presented data bring new insights into the mechanism how the phosphatidylinositol-3-kinase (PI3-K)/Akt pathway can influence migration of colorectal adenocarcinoma cells. Because FAK is indispensable for cell movements and functions downstream of Akt, our results imply FAK kinase as a potential key molecule during progression of tumors with active PI3-K/Akt signaling.
Identifiers
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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.