MiR-1290 targets CCNG2 to promote the metastasis of oral squamous cell carcinoma.

OBJECTIVE: MicroRNAs (miRNAs) have been demonstrated to be involved in the pathogenesis of various human cancers, including oral squamous cell carcinoma (OSCC). Here, we designed this study to explore the potential effect of miR-1290 on tumorigenesis of OSCC. PATIENTS AND METHODS: The expressions of miR-1290 and cyclin G2 (CCNG2) in OSCC were observed by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Dual-Luciferase Reporter Assay was performed to confirm the relationship between miR-1290 and CCNG2. The functions of miR-1290 and CCNG2 were analyzed using transwell assay. The Western blot analysis was used to detect epithelial-mesenchymal transition (EMT). RESULTS: Upregulation of miR-1290 and downregulation of CCNG2 were identified in OSCC. And upregulation of miR-1290 was associated with clinicopathological characteristics and poor prognosis in OSCC patients. Moreover, the downregulation of miR-1290 inhibited cell metastasis and EMT in OSCC cells. Furthermore, CCNG2 was a direct target of miR-1290. Its expression was inversely regulated by miR-1290 in OSCC cells. At the same time, the suppressive effect of CCNG2 was observed in OSCC. Furthermore, overexpression of CCNG2 weakened the promoted effect of miR-1290 on cell metastasis in OSCC. CONCLUSIONS: MiR-1290 promoted cell metastasis and EMT, inhibiting CCNG2 expression in OSCC.

MicroRNA-1246 expression associated with CCNG2-mediated chemoresistance and stemness in pancreatic cancer.

BACKGROUND: Pancreatic cancer has a poor prognosis because of its high refractoriness to chemotherapy and tumour recurrence, and these properties have been attributed to cancer stem cells (CSCs). MicroRNA (miRNA) regulates various molecular mechanisms of cancer progression associated with CSCs. This study aimed to identify the candidate miRNA and to characterise the clinical significance. METHODS: We established gemcitabine-resistant Panc1 cells, and induced CSC-like properties through sphere formation. Candidate miRNAs were selected through microarray analysis. The overexpression and knockdown experiments were performed by evaluating the in vitro cell growth and in vivo tumourigenicity. The expression was studied in 24 pancreatic cancer samples after laser captured microdissection and by immunohistochemical staining. RESULTS: The in vitro drug sensitivity of pancreatic cancer cells was altered according to the miR-1246 expression via CCNG2. In vivo, we found that miR-1246 could increase tumour-initiating potential and induced drug resistance. A high expression level of miR-1246 was correlated with a worse prognosis and CCNG2 expression was significantly lower in those patients. CONCLUSIONS: miR-1246 expression was associated with chemoresistance and CSC-like properties via CCNG2, and could predict worse prognosis in pancreatic cancer patients.

Cyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/ß-catenin signaling.

Estrogen plays an important role in the maintenance of bone formation, and deficiency in the production of estrogen is directly linked to postmenopausal osteoporosis. To date, the underlying mechanisms of estrogen-mediated osteogenic differentiation are not well understood. In this study, a pluripotent mesenchymal precursor cell line C2C12 was used to induce osteogenic differentiation and subjected to detection of gene expressions or to manipulation of cyclin G2 expressions. C57BL/6 mice were used to generate bilateral ovariectomized and sham-operated mice for analysis of bone mineral density and protein expression. We identified cyclin G2, an unconventional member of cyclin, is involved in osteoblast differentiation regulated by estrogen in vivo and in vitro. In addition, the data showed that ectopic expression of cyclin G2 suppressed expression of osteoblast transcription factor Runx2 and osteogenic differentiation marker genes, as well as ALP activity and in vitro extracellular matrix mineralization. Mechanistically, Wnt/ß-catenin signaling pathway is essential for cyclin G2 to inhibit osteogenic differentiation. To the best of our knowledge, the current study presents the first evidence that cyclin G2 serves as a negative regulator of both osteogenesis and Wnt/ß-catenin signaling. Most importantly, the basal and 17ß-estradiol-induced osteogenic differentiation was restored by overexpression of cyclin G2. These results taken together suggest that cyclin G2 may function as an endogenous suppressor of estrogen-induced osteogenic differentiation through inhibition of Wnt/ß-catenin signaling.

Change in expression of cyclin G2 in kidney cancer cell and its significance.

This study aims to analyze the expression and clinical significance of cyclin G2 (CCNG2) in kidney carcinoma, and the biological effect in its cell line by CCNG2 overexpression. Immunohistochemistry and western blot were used to analyze CCNG2 protein expression in 63 cases of kidney cancer and normal tissues to study the relationship between CCNG2 expression and clinical factors. CCNG2 lentiviral vector and empty vector were respectively transfected into kidney ACHN cell line. During immunohistochemistry, the level of CCNG2 protein expression was found to be significantly lower in kidney cancer tissue than normal tissues (P < 0.05). After Western blot, the relative amount of CCNG2 protein in kidney cancer tissue was respectively found to be significantly lower than in normal tissues (P < 0.05). The level of CCNG2 protein expression was not correlated with gender, age, tumor size, and pathological types (P > 0.05), but it was correlated with lymph node metastasis, clinic 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 show that ACHN cell-transfected CCNG2 had a lower survival fraction, higher percentage of the G0/G1 phases, and lower CDK2 protein expression compared with ACHN cell-untransfected CCNG2 (P < 0.05). CCNG2 expression decreased in kidney cancer and correlated significantly with lymph node metastasis, clinical stage, histological grade, and poor overall survival, suggesting that CCNG2 may play important roles as a negative regulator to kidney cancer ACHN cell by promoting degradation of CDK2.

CCNG2 expression is downregulated in colorectal carcinoma and its clinical significance.

This study aimed to analyze the expression, clinical significance of cyclin G2 (CCNG2) in colorectal carcinoma, and the biological effect in its cell line by CCNG2 overexpression. Immunohistochemistry and Western blot were used to analyze CCNG2 protein expression in colorectal cancer and to study the influence of the upregulated expression of CCNG2 that might be found on SW480 cell biological effect. We found that the level of CCNG2 protein expression was significantly lower in colorectal cancer tissue than normal tissues (P < 0.05). The level of CCNG2 was correlated with T stages, lymph node metastasis, clinic 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 has shown that SW480 cell-transfected CCNG2 had a lower survival fraction, higher percentage of the G0/G1 phases, and lower CDK2 protein expression compared with SW480 cell-untransfected CCNG2 (P < 0.05).

Changes in the expression of cyclin G2 in esophageal cancer cell and its significance.

This study aimed to analyze the expression, clinical significance of cyclin G2 (CCNG2) in esophageal carcinoma, and the biological effect in its cell line by CCNG2 overexpression. Immunohistochemistry and western blot were used to analyze CCNG2 protein expression in 73 cases of esophageal cancer and normal tissues to study the relationship between CCNG2 expression and clinical factors. CCNG2 lentiviral vector and empty vector were respectively transfected into esophageal cancer Eca-109 cell line. Reverse transcription-polymerase chain reaction 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 Eca-109 cell's biological effect. Immunohistochemistry: The level of CCNG2 protein expression was found to be significantly lower in esophageal cancer tissue than normal tissues (P < 0.05). Western blot: The relative amount of CCNG2 protein in esophageal cancer tissue was respectively found to be significantly lower than in normal tissues (P < 0.05). The level of CCNG2 protein expression was not correlated with gender, age, and tumor size (P > 0.05), but it was correlated with lymph node metastasis, clinic stage, and histological grades (P < 0.05). Loss of CCNG2 expression correlated significantly with poor overall survival time by Kaplan-Meier analysis. The result of the biological function showed that Eca-109 cell-transfected CCNG2 had a lower survival fraction, more percentage of the G0/G1 phases (P < 0.05), and lower cyclin-dependent kinase 2 (CDK2) protein expression. CCNG2 expression decreased in esophageal cancer and correlated significantly with lymph node metastasis, clinic stage, histological grade, and poor overall survival, suggesting that CCNG2 may play important roles as a negative regulator to esophageal cancer cell by promoting degradation of CDK2.

Effect of cyclin G2 on proliferative ability of prostate cancer PC-3 cell.

This study aimed to analyze the expression, clinical significance of cyclin G2 (CCNG2) in prostate carcinoma, and the biological effect in its cell line by CCNG2 overexpression. Immunohistochemistry and Western blot were used to analyze CCNG2 protein expression in 85 cases of prostate cancer and normal tissues to study the relationship between CCNG2 expression and clinical factors. CCNG2 lentiviral vector and empty vector were, respectively, transfected into prostate cancer PC-3 cell line. Reverse transcription-polymerase chain reaction (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 PC-3 cells biological effect. The level of CCNG2 protein expression was found to be significantly lower in prostate cancer tissue than normal tissues (P < 0.05). The level of CCNG2 protein expression was not correlated with age, PSA contention, and tumor size (P < 0.05), but it was correlated with lymph node metastasis, clinic stage, and Gleason score (P < 0.05). The result of biological function shown that PC-3 cell transfected CCNG2 had a lower survival fraction, more percentage of the G0/G1 phases, and lower CDK2 protein expression compared with PC-3 cell untransfected CCNG2 (P < 0.05). CCNG2 expression decreased in prostate cancer and correlated significantly with lymph node metastasis, clinic stage, and Gleason score, suggesting that CCNG2 may play important roles as a negative regulator to prostate cancer cell.