CCNG2 Suppressor Biological Effects on Thyroid Cancer Cell through Promotion of CDK2 Degradation

This study aimed to analyze the expression and clinical significance of cyclin G2 (CCNG2) in thyroid carcinomaand the biological effects of CCNG2 overexpression in a cell line. Immunohistochemistry and Western blottingwere used to analyze CCNG2 protein expression in 63 cases of thyroid cancer and normal tissues to allow therelationship with clinical factors to be assessed. CCNG2 lentiviral and empty vectors were transfected into thethyroid cancer K1 cell line. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blottingwere applied to detect the mRNA and protein levels of CCNG2. MTT assay and cell cycle were also conductedto assess the influence of up-regulated expression of CCNG2 on K1 cell biology. The level of CCNG2 proteinexpression was found to be significantly lower in thyroid cancer tissue than normal tissues (P<0.05). Westernblot: The relative amount of CCNG2 protein in thyroid cancer tissue was respectively found to be significantlylower than in normal tissues (P<0.05), correlating with lymph node metastasis, clinic stage and histological grade(P<0.05), but not gender, age or tumor size (P>0.05). Loss of CCNG2 expression correlated significantly withpoor overall survival time on Kaplan-Meier analysis (P<0.05). The results for biological functions showed thatK1 cell transfected CCNG2 had a lower survival fraction, a greater percentage in the G0/G1 phases, and lowercyclin-dependent kinase 2 (CDK2) protein expression compared with K1 cells non-transfected with CCNG2(P<0.05). CCNG2 expression decreased in thyroid cancer and correlated significantly lymph node metastasis,clinic stage, histological grade and poor overall survival, suggesting that CCNG2 may play important roles asa negative regulator in thyroid cancer K1 cells by promoting degradation of CDK2.