Journal
CANCERS
Volume 10, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/cancers10050139
Keywords
FAK; Pyk2; inflammation; carcinogenesis; metastasis; EMT
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Funding
- National Nature Science Foundation of China [81502105, 81672750]
- fund for the Key Laboratory of Higher Education Institutes of Shandong Province, China
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Focal adhesion kinase (FAK) and its homologous FAK-related proline-rich tyrosine kinase 2 (Pyk2) contain the same domain, exhibit high sequence homology and are defined as a distinct family of non-receptor tyrosine kinases. This group of kinases plays critical roles in cytoskeletal dynamics and cell adhesion by regulating survival and growth signaling. This review summarizes the physiological and pathological functions of Pyk2 in inflammation and cancers. In particular, overexpression of Pyk2 in cancerous tissues is correlated with poor outcomes. Pyk2 stimulates multiple oncogenic signaling pathways, such as Wnt/beta-catenin, PI3K/Akt, MAPK/ERK, and TGF-beta/EGFR/VEGF, and facilitates carcinogenesis, migration, invasion, epithelial-mesenchymal transition and metastasis. Therefore, Pyk2 is a high-value therapeutic target and has clinical significance.
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