ArticleMolecular cancer research : MCR2016
FAK Expression, Not Kinase Activity, Is a Key Mediator of Thyroid Tumorigenesis and Protumorigenic Processes.
Article in Molecular cancer research : MCR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Structure, Mutation, Functional Domain Roles and Medical Implications of Glycerol Kinase.The protein journal · 2026Review
- Focal adhesion kinase promotes ribosome biogenesis to drive advanced thyroid cancer cell growth and survival.Frontiers in oncology · 2025Article
- Cancer-associated fibroblast-derived periostin promotes papillary thyroid tumor growth through integrin-FAK-STAT3 signaling.Theranostics · 2024Article
- Focal adhesion kinase: from biological functions to therapeutic strategies.Experimental hematology & oncology · 2023Review
- Fibronectin Contributes to a BRAF Inhibitor-driven Invasive Phenotype in Thyroid Cancer through EGR1, Which Can Be Blocked by Inhibition of ERK1/2.Molecular cancer research : MCR · 2023Article
- Design, synthesis, and biological evaluation of potent FAK-degrading PROTACs.Journal of enzyme inhibition and medicinal chemistry · 2022Article
- Focal adhesion kinase splicing and protein activation in papillary thyroid carcinoma progression.Histochemistry and cell biology · 2022Article
- Molecularly Guided Drug Repurposing for Cholangiocarcinoma: An Integrative Bioinformatic Approach.Genes · 2022Article
- Identification and Validation of Esophageal Squamous Cell Carcinoma Targets for Fluorescence Molecular Endoscopy.International journal of molecular sciences · 2021Article
- Article
- Novel nomogram to predict risk of bone metastasis in newly diagnosed thyroid carcinoma: a population-based study.BMC cancer · 2020Article
- Design, Synthesis, and Evaluation of Highly Potent FAK-Targeting PROTACs.ACS medicinal chemistry letters · 2020Article
- The Thyroid Tumor Microenvironment: Potential Targets for Therapeutic Intervention and Prognostication.Hormones & cancer · 2020Review
- Bone metastases in thyroid cancer.Journal of bone oncology · 2020Review
- Development of a High-Throughput Fluorescence Polarization Assay to Detect Inhibitors of the FAK-Paxillin Interaction.SLAS discovery : advancing life sciences R & D · 2020Article
- Inhibition of protein FAK enhances 5-FU chemosensitivity to gastric carcinomaComputational and structural biotechnology journal · 2020Article
- Activation of the IGF Axis in Thyroid Cancer: Implications for Tumorigenesis and Treatment.International journal of molecular sciences · 2019Review
- Establishment and Characterization of Four Novel Thyroid Cancer Cell Lines and PDX Models Expressing the RET/PTC1 Rearrangement, BRAFV600E, or RASQ61R as Drivers.Molecular cancer research : MCR · 2019Article
- Article
- Sphingosine kinase 1 promotes the metastasis of colorectal cancer by inducing the epithelial‑mesenchymal transition mediated by the FAK/AKT/MMPs axis.International journal of oncology · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledThere are limited therapy options for advanced thyroid cancer, including papillary and anaplastic thyroid cancer (PTC and ATC). Focal adhesion kinase (FAK) regulates cell signaling by functioning as a scaffold and kinase. Previously, we demonstrated that FAK is overexpressed and activated in thyroid cancer cells and human PTC clinical specimens. However, it remains unclear whether patients with advanced thyroid cancer will benefit from FAK inhibition. Therefore, the dual functions of FAK in mediating protumorigenic processes and thyroid tumorigenesis were investigated. Evidence here shows that FAK expression predominantly regulates thyroid cancer cell growth, viability, and anchorage-independent growth. FAK inhibition, with PF-562,271 treatment, modestly reduced tumor volumes, while FAK depletion, through shRNA knockdown, significantly reduced tumor volumes in vivo A role for FAK expression in tumor establishment was demonstrated in a model of PTC, where FAK knockdown tumors did not develop. FAK depletion also led to a significant decrease in overall metastatic burden. Interestingly, pretreatment with a FAK inhibitor resulted in a paradoxical increase in metastasis in a model of ATC, but decreased metastasis in a model of PTC. These data provide the first evidence that FAK expression is critical for the regulation of thyroid tumorigenic functions. IMPLICATIONS: This study demonstrates that FAK expression, but not kinase activity alone, predominantly mediates thyroid tumor growth and metastasis, indicating that targeting the scaffolding function(s) of FAK may be an important therapeutic strategy for advanced thyroid cancer, as well as other FAK-dependent tumors. Mol Cancer Res; 14(9); 869-82. ©2016 AACR.
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