Focal adhesion kinase (FAK) is a non‐receptor tyrosine kinase and involves in regulating cell adhesion, motility, proliferation and survival. Previous studies demonstrated that 3’‐deoxyadenosine (also known as cordycepin) suppressed the expression of integrins and FAK as well as cell migration and epithelial‐mesenchymal transition in the hepatocellular carcinoma. However, the mechanism that cordycepin influences FAK expression and angiogenesis in the endothelial cells (ECs) remains unclear. In this study, we found that cordycepin suppresses FAK expression and phosphorylation of FAK at Tyr397 in human umbilical vein, coronary artery and pulmonary artery endothelial cells. Intriguingly, the result from the analysis of confocal microscopy reveals that cordycepin reduces the expression of FAK in the cytoplasm but not in the focal adhesions. In addition, cordycepin inhibits cell proliferation, wound healing, trans‐well cell migration and tube formation of ECs. Moreover, we found that cordycepin induces p53 and p21 expression resulting in G1 cell cycle arrest. Finally, we demonstrate that cordycepin suppresses angiogenesis via the in vivo angiogenesis assay and reduces tumor growth in a xenograft nude mice model. Taken together, our study indicated that cordycepin attenuates cell proliferation and migration which may result in impairment of angiogenesis process and tumor growth via downregulation of FAK expression and induction of p53 and p21 in ECs. As a result, cordycepin could be considered as a potential adjuvant for cancer therapy.
Date:
2016-12
Relation:
Molecular Biology of the Cell. 2016 Dec;27:Meeting Abstract P1104.
