Proline-Rich Protein Tyrosine Kinase 2 in Inflammation and Cancer.
Xiangdong ZhuYonghua BaoYongchen GuoWancai YangPublished in: Cancers (2018)
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/β-catenin, PI3K/Akt, MAPK/ERK, and TGF-β/EGFR/VEGF, and facilitates carcinogenesis, migration, invasion, epithelial⁻mesenchymal transition and metastasis. Therefore, Pyk2 is a high-value therapeutic target and has clinical significance.
Keyphrases
- tyrosine kinase
- pi k akt
- signaling pathway
- epithelial mesenchymal transition
- cell proliferation
- epidermal growth factor receptor
- cell adhesion
- transforming growth factor
- cell migration
- oxidative stress
- cell cycle arrest
- induced apoptosis
- papillary thyroid
- gene expression
- transcription factor
- dna damage
- stem cells
- vascular endothelial growth factor
- metabolic syndrome
- squamous cell carcinoma
- endothelial cells
- escherichia coli
- small cell lung cancer
- type diabetes
- free survival
- protein kinase
- cystic fibrosis
- young adults
- amino acid
- protein protein