Abstract
Proline-rich tyrosine kinase 2 (Pyk2), a member of the focal adhesion kinase family, has recently been associated with tumor development. However, the role of Pyk2 in renal cell carcinoma (RCC) remains unexplored. The present study investigated the expression pattern, clinical significance, and function of Pyk2 in RCC. By using a reverse transcription-quantitative polymerase chain reaction, tissue microarray and immunohistochemistry, it was demonstrated that RCC tissues display a higher Pyk2 expression compared with paired adjacent nontumor tissues. Furthermore, it was revealed that Pyk2 upregulation was associated with poor clinical outcomes in patients with RCC. By using loss-of-function approaches, it was demonstrated that Pyk2 knockdown reduced cell viability, invasive ability and migratory ability, and increased apoptosis in RCC cell lines. In contrast, Pyk2 overexpression promoted tumor cell proliferation, invasion and migration and reduced apoptosis. Collectively, the results of the present study present the tumor-promoting function of Pyk2 in RCC and thus provide molecular evidence for novel tyrosine kinase inhibitors as novel therapeutic options for RCC.