ArticleThe Journal of biological chemistry2013
Function of focal adhesion kinase scaffolding to mediate endophilin A2 phosphorylation promotes epithelial-mesenchymal transition and mammary cancer stem cell activities in vivo.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 75 citations in OpenAlex.
- AKAP2 is required for assembly of cytoskeletal signaling complexes that promote growth and metastasis of triple-negative breast cancer.The Journal of biological chemistry · 2026Article
- Polydopamine-Coated Surfaces Promote Adhesion, Migration, Proliferation, Chemoresistance, Stemness, and Epithelial-Mesenchymal Transition of Human Prostate Cancer Cell Lines In Vitro via Integrin αInternational journal of molecular sciences · 2026Article
- Database analysis reveals endophilin A expression as a marker of metastasis and prognosis in breast cancer.Discover oncology · 2025Article
- Bending the boundaries: the many facets of endophilin-As from membrane dynamics to disease.Cellular and molecular life sciences : CMLS · 2025Review
- Targeting FAK to Potentiate Immune Checkpoint Therapy in Solid Tumors.Journal of cancer immunology · 2025Article
- Identification and experimental validation of a sialylation-related long noncoding RNA signature for prognosis of bladder cancer.BMC urology · 2024Article
- Focal adhesion kinase: from biological functions to therapeutic strategies.Experimental hematology & oncology · 2023Review
- Endocytosis in cancer and cancer therapy.Nature reviews. Cancer · 2023Review
- An m7G-related lncRNA signature predicts prognosis and reveals the immune microenvironment in bladder cancer.Scientific reports · 2023Article
- Focal adhesion kinase inhibitors prevent osteoblast mineralization in part due to suppression of Akt-mediated stabilization of osterix.Journal of bone oncology · 2022Article
- Gut homeostasis, injury, and healing: New therapeutic targets.World journal of gastroenterology · 2022Review
- FAK in Cancer: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2022Review
- Multi-layered proteogenomic analysis unravels cancer metastasis directed by MMP-2 and focal adhesion kinase signaling.Scientific reports · 2021Article
- Targeted protein degradation: A promise for undruggable proteins.Cell chemical biology · 2021Review
- Review
- Endophilin A2-mediated alleviation of endoplasmic reticulum stress-induced cardiac injury involves the suppression of ERO1α/IPInternational journal of biological sciences · 2021Article
- Vimentin filaments drive migratory persistence in polyploidal cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Radiosensitization by Kinase Inhibition Revealed by Phosphoproteomic Analysis of Pancreatic Cancer Cells.Molecular & cellular proteomics : MCP · 2020Article
- Expression of ASAP1 and FAK in gastric cancer and its clinicopathological significance.Oncology letters · 2020Article
- Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
Tyrosine kinases have been shown to play critical roles in cancer development and progression, and their inhibitors hold the potential as effective targeted therapies for breast and other cancers. However, some of these kinases like focal adhesion kinase (FAK) also possess scaffolding functions in intracellular signaling, but such kinase-independent functions of FAK or other kinases have not been examined in cancer directly in vivo. Here, we report that disruption of the function of FAK scaffolding through its Pro-878/881 motif suppressed mammary tumor growth and metastasis in a well characterized murine model of human breast cancer. P878A/P881A mutation in the endogenous FAK gene decreased the expression of markers for epithelial-mesenchymal transition (EMT) and mammary cancer stem cell (MaCSC) activities in tumors derived from mutant mice. This mutation disrupted the function of FAK scaffolding to mediate endophilin A2 phosphorylation at Tyr-315 by Src, leading to the decreased surface expression of MT1-MMP, as observed previously in transformed fibroblasts in vitro. Inhibition of the downstream components of this FAK scaffolding function by Y315F endophilin A2 mutant or MT1-MMP knockdown reduced markers for EMT and MaCSC activities. Conversely, bypass of the scaffolding function using the phosphorylation mimic mutant Y315E endophilin A2 or endophilin A2 knockdown rescued the decreased markers for EMT and MaCSCs as well as surface expression of MT1-MMP in tumor cells harboring the P878A/P881A mutation. Together, these results identify a novel role of FAK scaffolding function in breast cancer, which could serve as a new target in combination with kinase inhibition for more effective treatment strategies.
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