• Asian Pacific Journal of Cancer Prevention
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• v.14 no.10
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• pp.6165-6171
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• 2013

This study aimed to analyze the expression and clinical significance of cyclin G2 (CCNG2) in thyroid carcinoma and the biological effects of CCNG2 overexpression in a cell line. Immunohistochemistry and Western blotting were used to analyze CCNG2 protein expression in 63 cases of thyroid cancer and normal tissues to allow the relationship with clinical factors to be assessed. CCNG2 lentiviral and empty vectors were transfected into the thyroid cancer K1 cell line. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were applied to detect the mRNA and protein levels of CCNG2. MTT assay and cell cycle were also conducted to assess the influence of up-regulated expression of CCNG2 on K1 cell biology. The level of CCNG2 protein expression was found to be significantly lower in thyroid cancer tissue than normal tissues (P<0.05). Western blot: The relative amount of CCNG2 protein in thyroid cancer tissue was respectively found to be significantly lower 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 with poor overall survival time on Kaplan-Meier analysis (P<0.05). The results for biological functions showed that K1 cell transfected CCNG2 had a lower survival fraction, a greater percentage in the G0/G1 phases, and lower cyclin-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 as a negative regulator in thyroid cancer K1 cells by promoting degradation of CDK2.

• Animal cells and systems
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• v.12 no.1
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• pp.15-21
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• 2008

Nitric oxide(NO) has been known to play important roles in numerous physiologic processes including neurotransmission, vasorelaxation, and cellular apoptosis. Using a mouse cDNA gene chip, we examined expression patterns and time course of NO-dependent genes in mouse macrophage RAW264.7 cells. Genes shown to be upregulated more than two fold or at least at two serial time points were further selected and validated by RT-PCR. Finally, 81 selected genes were classified by function as signaling, apoptosis, inflammation, transcription, translation, ionic homeostasis and metabolism. Among those, genes related with signaling, apoptosis and inflammation, such as guanylate cyclase 1, soluble, alpha3(Gucy1a3); protein kinase C, alpha($Pkc{\alpha}$); lymphocyte protein tyrosine kinase(Lck); BCL2/adenovirus E1B 19 kDa-interacting protein(Bnip3); apoptotic protease activating factor 1(Apaf1); X-linked inhibitor of apoptosis(Xiap); cyclin G1(Ccng1); chemokine(C-C motif) ligand 4(Ccl4); B cell translocation gene 2, anti-proliferative(Btg2); lysozyme 2(Lyz2); secreted phosphoprotein 1(Spp1); heme oxygenase(decycling) 1(Hmox1); CD14 antigen(Cd14); and granulin(Grn) may play important roles in NO-dependent responses in murine macrophages.