The role of Pyk2 in the CCR7-mediated regulation of metastasis and viability in squamous cell carcinoma of the head and neck cells in vivo and in vitro.

In the present study, we aimed to demonstrate whether praline-rich tyrosine kinase-2 (Pyk2) participates in the chemokine receptor 7 (CCR7) downstream signaling network, and to determine the role of this molecule and the related mechanism in the CCR7-mediated regulation of viability and metastasis in vivo and in vitro of squamous cell carcinoma of the head and neck (SCCHN). We constructed the stable Pyk2 related non-kinase (PRNK)-expressing SCCHN cell line, and examined the viability, apoptosis, migration, invasion and adhesion ability in the transfected and untransfected SCCHN cells. An SCCHN tumor model in nude mice was designed and the tumor growth rate was assayed. E-cadherin and vimentin expression was assessed when Pyk2 was inactivated. We found that the stable PRNK-expressing SCCHN cells exhibited low viability, a high rate of apoptosis, low migratory ability, low invasive ability and low adhesion capacity. In the nude mouse body, the tumors formed by these cells grew slowly when compared to the tumor growth in the control group. When Pyk2 was inactivated, CCR7-induced E-cadherin and vimentin expression levels were altered. Thus, Pyk2 is a key downstream signaling molecules of CCR7 in SCCHN, which promotes SCCHN tumorigenesis and progression.