4.1 Article

Decreased expression of CCNG2 is significantly linked to the malignant transformation of gastric carcinoma

Journal

TUMOR BIOLOGY
Volume 35, Issue 3, Pages 2631-2639

Publisher

SAGE PUBLICATIONS LTD
DOI: 10.1007/s13277-013-1346-2

Keywords

CCNG2; Gastric cancer; Prognosis; Tumor metastasis

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This study aimed to analyze the expression, clinical significance of cyclin G2 (CCNG2) in gastric carcinoma, and the biological effect in its cell line by CCNG2 overexpression. Immunohistochemistry and western blot were used to analyze CCNG2 protein expression in 87 cases of gastric cancer and normal tissues to study on the relationship between CCNG2 expression and clinical factors. CCNG2 lentiviral vector was transfected into gastric SGC-7901 cell line. RT-PCR and western blot were used to detect the mRNA level and protein of CCNG2. MTT assay and cell cycle were also conducted as to the influence of the upregulated expression of CCNG2 that might be found on SGC-7901 cell biological effect. Immunohistochemically, the level of CCNG2 protein expression was found to be significantly lower in gastric cancer tissue than in normal tissues (P < 0.05). Western blot shows that the relative amount of CCNG2 protein in gastric cancer tissue was found to be significantly lower than in normal tissues (P < 0.05). The level of CCNG2 protein expression was correlated with T stages, lymph node metastasis, clinical stage, and histological grade (P < 0.05). Loss of CCNG2 expression correlated significantly with poor overall survival time by Kaplan-Meier analysis (P < 0.05). The result of biological function showed that SGC-7901 cell-transfected CCNG2 had a lower survival fraction, higher percentage of the G0/G1 phases, and lower CDK2 protein expression compared with SGC-7901 cell untransfected CCNG2 (P < 0.05). CCNG2 expression decreased in gastric cancer and correlated significantly T stages, lymph node metastasis, clinical stage, histological grade, and poor overall survival, suggesting that CCNG2 may play important roles as a negative regulator to gastric cancer cell by promoting degradation of CDK2.

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