High expression of CHEK2 promotes tumor progression in kidney renal clear cell carcinoma through targeting TEAD4 signaling pathway.

Emerging evidence indicated that CHEK2 played crucial functions in the development of several cancers. However, its role in kidney renal clear cell carcinoma (KIRC) is still remained unclear. The present study was designed to investigate the prognostic value and biological function of CHEK2 in KIRC. To investigate CHEK2's expression in KIRC, raw gene expression data were downloaded from the GEO database. Western blot was performed to validate the expression level of CHEK2 in twelve pairs of KIRC tumor tissues. Immunohistochemistry (IHC) analyses based on clinical samples were employed to verify the relationship between CHEK2 expression and KIRC malignancy. MTT, wound healing, and transwell assay were conducted to explore CHEK2's biological functions. The xenograft models were used to explore the function of CHEK2 in vivo. CHEK2 expression was up-regulated in KIRC tumors, and high expression of CHEK2 was significantly correlated with advanced TNM stages and poor prognosis. Functional studies demonstrated that up-regulation of CHEK2 promoted cancer cell aggressiveness, including cell proliferation, migration, and invasion. Subsequent evidence proved that TEAD4/RUNX1 is the downstream effector for CHEK2-mediated KIRC malignancy. CHEK2 was identified as a novel biomarker to predict the prognosis and tumor progression in KIRC, and a promising therapeutic target to prevent tumor progression.