Objective To examine the expression of cell division cycle associated 2(CDCA 2) in pancreatic ductal adenocarcinoma(PDAC) and investigate its role in prognosis of PDAC patients.Methods This retrospective study include...Objective To examine the expression of cell division cycle associated 2(CDCA 2) in pancreatic ductal adenocarcinoma(PDAC) and investigate its role in prognosis of PDAC patients.Methods This retrospective study included 155 PDAC patients who underwent surgical treatment and complete post-operative follow-up.Clinicopathologic data were collected through clinical database.Tissue microarray was constructed and immunohistochemistry was performed to detect CDCA2 expression in the PDAC tumor tissues and adjacent non-tumor tissues.Clinicopathological characteristics between high and low CDCA2 expression were compared.Correlation of CDCA2 expressions with patients' survival was analyzed using Kaplan-Meier method and Cox regression analysis.Results Expression of CDCA2 in PDAC cells was significantly higher than that in adjacent non-tumor tissues(U=4056.5,P<0.001).Univariate analysis showed that CDCA2 expression [hazard ratio(HR)=1.574,95% confidence interval(CI)=1.014-2.443,P=0.043] and node metastasis(HR=1.704,95%CI=1.183-2.454,P=0.004) were significantly associated with prognosis.Cox regression analysis showed CDCA2 expression was not an independent prognostic risk factor(HR=1.418,95%CI=0.897-2.242,P=0.135) for PDCA patients.Stratification survival analysis demonstrated CDCA2 expression as an independent prognostic risk factor in male patients(HR=2.554,95%CI=1.446-4.511,P=0.003) or in non-perineural invasion patients(HR=2.290,95%CI=1.146-4.577,P=0.012).Conclusions CDCA2 is highly expressed in PDAC tumor tissue.Although CDCA2 is not an independent prognostic risk factor for PDAC patients,it might be used to help predict prognosis of male or non-perineural invasion patients of PDAC.展开更多
To the Editor:Kinase cell division cycle 7(CDC7),a cell division cycle protein,takes a vital role in mediating DNA replication1.CDC7 complexes in the nucleus can phosphorylate the minichromosome maintenance complex(MC...To the Editor:Kinase cell division cycle 7(CDC7),a cell division cycle protein,takes a vital role in mediating DNA replication1.CDC7 complexes in the nucleus can phosphorylate the minichromosome maintenance complex(MCM)family members that bind to chromosomes.In addition,CDC7 kinase,as a molecular switch regulating DNA replication,can mediate DNA damage signaling pathways to stimulate cell cycle termination as well as DNA replication2.Studies have shown that CDC7 is overexpressed in many types of cancer cells,and its overexpression was related to poor patient survival,tumor grade,genetic instability,aneuploidy and so on3.Therefore,CDC7 is a promising target for antitumor therapy.展开更多
Bone morphogenetic protein-7 is widely accepted as an inducer for bone marrow stem cells differentiating into osteoblasts and chondrocytes. Whether bone marrow stromal cells differentiate into neuron-like cells remain...Bone morphogenetic protein-7 is widely accepted as an inducer for bone marrow stem cells differentiating into osteoblasts and chondrocytes. Whether bone marrow stromal cells differentiate into neuron-like cells remains unclear. The current study examined the presence of positive cells for intermediate filament protein and microtubule associated protein-2 in the cytoplasm of bone marrow stromal cells induced by bone morphogenetic protein-7 under an inverted microscope, while no expression of glial fibrillary acidic protein was found. Reverse transcription PCR electrophoresis also revealed a positive target band for intermediate filament protein and microtubule-associated protein 2 mRNA. These results confirmed that bone morphogenetic protein-7 induces rat bone marrow stromal cells differentiating into neuron-like cells.展开更多
AIM:To explore the role of S-phase kinase-associated protein-2(Skp2)in gallbladder carcinoma and to identify whether depletion of Skp2 by Skp2-RNAi could attenuate proliferation and migration of gallbladder carcinoma....AIM:To explore the role of S-phase kinase-associated protein-2(Skp2)in gallbladder carcinoma and to identify whether depletion of Skp2 by Skp2-RNAi could attenuate proliferation and migration of gallbladder carcinoma.METHODS:Skp2-RNAi was transduced into cells of the gallbladder carcinoma cell line GBC-SD,using a lentiviral vector.The effect of Skp2-RNAi on the proliferation,migration,invasion and cell cycle of GBC-SD cells was studied using in vitro assays for cell proliferation,colony formation,wound healing and cell cycle.The expression of Skp2 and p27 was detected by real-time polymerase chain reaction and Western immunoblotting.The effect of Skp2-RNAi on the proliferation of GBC-SD cells in vivo was investigated by tumorigenicity experiments in nude mice.RESULTS:Lentivirus-mediated RNAi reduced the expression of Skp2 in cultured cells.The expression of the p27 protein increased along with the down-regulation of Skp2,although no significant difference was found in p27 mRNA expression.Flow cytometry revealed that Skp2-RNAi transfection significantly increased the proportion of cells in the S phase and significantly decreased the proportion of cells in the G 2 /M phase.No significant difference in the frequency of cells in the G0/G1 phase was observed.The results from the cell proliferation,colony formation and wound healing assays revealed that Skp2-RNAi transfection markedly inhibited the proliferation and migration of GBC-SD cells in vitro.Additionally,tumorigenicity experiments showed that suppression of Skp2 significantly decreased the weights of the tumors(0.56 ± 0.11 and 0.55 ± 0.07 g in the control and Scr-RNAi groups vs 0.37 ± 0.09 and 0.35 ± 0.08 g in the Skp2-RNAi-L and Skp2-RNAi-H groups).CONCLUSION:The expression of Skp2 in GBC-SD cells was inhibited following Skp2-RNAi transfection.Silencing of the Skp2 gene inhibited proliferation,migration and invasiveness of GBC-SD cells by mechanisms dependent on enhanced expression of the p27 protein.展开更多
基金Supported by the National High Technology Research and Development Program of China(863 Program)(2012AA02A212)
文摘Objective To examine the expression of cell division cycle associated 2(CDCA 2) in pancreatic ductal adenocarcinoma(PDAC) and investigate its role in prognosis of PDAC patients.Methods This retrospective study included 155 PDAC patients who underwent surgical treatment and complete post-operative follow-up.Clinicopathologic data were collected through clinical database.Tissue microarray was constructed and immunohistochemistry was performed to detect CDCA2 expression in the PDAC tumor tissues and adjacent non-tumor tissues.Clinicopathological characteristics between high and low CDCA2 expression were compared.Correlation of CDCA2 expressions with patients' survival was analyzed using Kaplan-Meier method and Cox regression analysis.Results Expression of CDCA2 in PDAC cells was significantly higher than that in adjacent non-tumor tissues(U=4056.5,P<0.001).Univariate analysis showed that CDCA2 expression [hazard ratio(HR)=1.574,95% confidence interval(CI)=1.014-2.443,P=0.043] and node metastasis(HR=1.704,95%CI=1.183-2.454,P=0.004) were significantly associated with prognosis.Cox regression analysis showed CDCA2 expression was not an independent prognostic risk factor(HR=1.418,95%CI=0.897-2.242,P=0.135) for PDCA patients.Stratification survival analysis demonstrated CDCA2 expression as an independent prognostic risk factor in male patients(HR=2.554,95%CI=1.446-4.511,P=0.003) or in non-perineural invasion patients(HR=2.290,95%CI=1.146-4.577,P=0.012).Conclusions CDCA2 is highly expressed in PDAC tumor tissue.Although CDCA2 is not an independent prognostic risk factor for PDAC patients,it might be used to help predict prognosis of male or non-perineural invasion patients of PDAC.
基金Zenji Research Laboratories for financial aid to this work
文摘To the Editor:Kinase cell division cycle 7(CDC7),a cell division cycle protein,takes a vital role in mediating DNA replication1.CDC7 complexes in the nucleus can phosphorylate the minichromosome maintenance complex(MCM)family members that bind to chromosomes.In addition,CDC7 kinase,as a molecular switch regulating DNA replication,can mediate DNA damage signaling pathways to stimulate cell cycle termination as well as DNA replication2.Studies have shown that CDC7 is overexpressed in many types of cancer cells,and its overexpression was related to poor patient survival,tumor grade,genetic instability,aneuploidy and so on3.Therefore,CDC7 is a promising target for antitumor therapy.
基金Science and Technology Research and Development Program of Shihezi University, No. ZRKX2009YB23
文摘Bone morphogenetic protein-7 is widely accepted as an inducer for bone marrow stem cells differentiating into osteoblasts and chondrocytes. Whether bone marrow stromal cells differentiate into neuron-like cells remains unclear. The current study examined the presence of positive cells for intermediate filament protein and microtubule associated protein-2 in the cytoplasm of bone marrow stromal cells induced by bone morphogenetic protein-7 under an inverted microscope, while no expression of glial fibrillary acidic protein was found. Reverse transcription PCR electrophoresis also revealed a positive target band for intermediate filament protein and microtubule-associated protein 2 mRNA. These results confirmed that bone morphogenetic protein-7 induces rat bone marrow stromal cells differentiating into neuron-like cells.
文摘AIM:To explore the role of S-phase kinase-associated protein-2(Skp2)in gallbladder carcinoma and to identify whether depletion of Skp2 by Skp2-RNAi could attenuate proliferation and migration of gallbladder carcinoma.METHODS:Skp2-RNAi was transduced into cells of the gallbladder carcinoma cell line GBC-SD,using a lentiviral vector.The effect of Skp2-RNAi on the proliferation,migration,invasion and cell cycle of GBC-SD cells was studied using in vitro assays for cell proliferation,colony formation,wound healing and cell cycle.The expression of Skp2 and p27 was detected by real-time polymerase chain reaction and Western immunoblotting.The effect of Skp2-RNAi on the proliferation of GBC-SD cells in vivo was investigated by tumorigenicity experiments in nude mice.RESULTS:Lentivirus-mediated RNAi reduced the expression of Skp2 in cultured cells.The expression of the p27 protein increased along with the down-regulation of Skp2,although no significant difference was found in p27 mRNA expression.Flow cytometry revealed that Skp2-RNAi transfection significantly increased the proportion of cells in the S phase and significantly decreased the proportion of cells in the G 2 /M phase.No significant difference in the frequency of cells in the G0/G1 phase was observed.The results from the cell proliferation,colony formation and wound healing assays revealed that Skp2-RNAi transfection markedly inhibited the proliferation and migration of GBC-SD cells in vitro.Additionally,tumorigenicity experiments showed that suppression of Skp2 significantly decreased the weights of the tumors(0.56 ± 0.11 and 0.55 ± 0.07 g in the control and Scr-RNAi groups vs 0.37 ± 0.09 and 0.35 ± 0.08 g in the Skp2-RNAi-L and Skp2-RNAi-H groups).CONCLUSION:The expression of Skp2 in GBC-SD cells was inhibited following Skp2-RNAi transfection.Silencing of the Skp2 gene inhibited proliferation,migration and invasiveness of GBC-SD cells by mechanisms dependent on enhanced expression of the p27 protein.
