title: CCNG2 suppressor biological effects on thyroid cancer cell through promotion of CDK2 degradation.
abstract: 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.
authors.affiliation: Department of Endocrinology (Section I), Tangshan Workers Hospital, Tangshan, China E-mail : weijuan_li2013@163.com.
authors.forename: Wei-Juan
authors.initials: WJ
authors.lastname: Li
authors.forename: Ge-Ling
authors.initials: GL
authors.lastname: Liu
authors.forename: Fang
authors.initials: F
authors.lastname: Yu
authors.forename: Xiu-Xiu
authors.initials: XX
authors.lastname: Xiang
authors.forename: Yi-Fang
authors.initials: YF
authors.lastname: Lu
authors.forename: Hong-Zhen
authors.initials: HZ
authors.lastname: Xiao
authors.forename: Yan-Ping
authors.initials: YP
authors.lastname: Shi
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics / Q000378:metabolism* / Q000556:secondary; D000328:Adult; D000368:Aged; D017209:Apoptosis; D015153:Blotting, Western; D049109:Cell Proliferation; D056767:Cyclin G2 / Q000235:genetics / Q000378:metabolism*; D051357:Cyclin-Dependent Kinase 2 / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007124:Immunoenzyme Techniques; D008207:Lymphatic Metastasis; D008297:Male; D008875:Middle Aged; D059748:Proteolysis; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013961:Thyroid Gland / Q000378:metabolism*; D013964:Thyroid Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D014407:Tumor Cells, Cultured
chemical_list: C101593:CCNG2 protein, human; D056767:Cyclin G2; D012333:RNA, Messenger; C495894:CDK2 protein, human; D051357:Cyclin-Dependent Kinase 2