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1.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 707-12, 2012.
Article in English | WPRIM | ID: wpr-636623

ABSTRACT

This study examined the possible role of p120ctn in the pathogenesis and development of pancreatic cancer. PANC-1 cells, a kind of human pancreatic carcinoma cell line, were cultured in this study. p120ctn was immunocytochemically detected in PANC-1 cells. The recombinant lentivirus vector was constructed to knock down the p120ctn expression of PANC-1 cells. Real-time quantitative PCR (RQ-PCR) and Western blotting were used to determine the expression of p120ctn and E-cadherin in PANC-1 cells after p120ctn knockdown. The adhesion, invasion and migration capacity of PANC-1 cells after p120ctn knockdown was detected by cell adhesion, invasion and migration assays. Cell growth was measured by the MTT method. Cell cycle and apoptosis were analyzed by fluorescence-activated cell sorting. The results showed that p120ctn knockdown led to significantly down-regulated E-cadherin and a reduced cell-to-cell adhesion ability in PANC-1 cells. shRNA-mediated knockdown of p120ctn reduced invasion and migration capacity of PANC-1 cells, inhibited cell growth, caused a significant decrease in the percentage of cells in G(1), an increase in S, and promoted apoptosis of PANC-1 cells. It was concluded that p120ctn plays a pivotal role in the proliferation and metastasis of pancreatic carcinoma, suggesting that p120ctn is a novel target for pancreatic carcinoma treatment.

2.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 707-712, 2012.
Article in English | WPRIM | ID: wpr-233095

ABSTRACT

This study examined the possible role of p120ctn in the pathogenesis and development of pancreatic cancer. PANC-1 cells, a kind of human pancreatic carcinoma cell line, were cultured in this study. p120ctn was immunocytochemically detected in PANC-1 cells. The recombinant lentivirus vector was constructed to knock down the p120ctn expression of PANC-1 cells. Real-time quantitative PCR (RQ-PCR) and Western blotting were used to determine the expression of p120ctn and E-cadherin in PANC-1 cells after p120ctn knockdown. The adhesion, invasion and migration capacity of PANC-1 cells after p120ctn knockdown was detected by cell adhesion, invasion and migration assays. Cell growth was measured by the MTT method. Cell cycle and apoptosis were analyzed by fluorescence-activated cell sorting. The results showed that p120ctn knockdown led to significantly down-regulated E-cadherin and a reduced cell-to-cell adhesion ability in PANC-1 cells. shRNA-mediated knockdown of p120ctn reduced invasion and migration capacity of PANC-1 cells, inhibited cell growth, caused a significant decrease in the percentage of cells in G(1), an increase in S, and promoted apoptosis of PANC-1 cells. It was concluded that p120ctn plays a pivotal role in the proliferation and metastasis of pancreatic carcinoma, suggesting that p120ctn is a novel target for pancreatic carcinoma treatment.


Subject(s)
Humans , Catenins , Genetics , Cell Line, Tumor , Gene Silencing , Pancreatic Neoplasms , Genetics
3.
International Journal of Surgery ; (12): 672-675, 2008.
Article in Chinese | WPRIM | ID: wpr-398341

ABSTRACT

Objective To compare the effects of laparoscopic cholecystectomy and laparoscopic common bile duct exploration combined choledochoscopic exploration( method A)and duodenoscopic sphincterotomy combined with laparoscopic cholecystectomy( method B) in treating choledocholithiasis with cholecystohthia-sis. Methods A retrospective study was adopted to analyze by statistical methods comparatively the clinical data of 114 patients, concerning operation time, blood lost, odynolysis rate, conversion rate,calculi residual rate ,complication rate ,hospitalization time and cost, et al. 68 cases were treated by method A,and 72 ca-ses were treated by method B. Results There were statistical differences in calculi residual rate, a conver-sion rate, apart complication rates and hospitalization cost between two groups, but there was no statistical difference in other index. Conclusion The two methods for choledocholithiasis and cholecystohthiasis has advantage and shortcoming respectively. The treatment for patients must be individualized by MRCP/USG, actual state of illness, and so on.

4.
Chinese Journal of Pathophysiology ; (12): 2012-2017, 2007.
Article in Chinese | WPRIM | ID: wpr-404465

ABSTRACT

AIM:To investigate the construction of oligonucleotide microarray specialized for pancreatic adenocarcinoma-associated genes and its preliminary application of detecting differential expressed genes in pancreatic cancer.METHODS:Pancreatic cancer related genes were purposely selected,and oligonucleotide microarray was prepared by spotting oligonucleotide probes on glass slides coated with APS-PDC.Labeled cDNA targets for hybridizations were synthesized by reverse transcription from total RNA in the presence of Cy5-dCTP and Cy3-dCTP,respectively.Hybridized microarray was scanned by Agilent laser scanner,and the aquired image was analyzed by Imagene3.0 software.The intensity ratios of Cy3 and Cy5 were calculated.To confirm the expression profiles of these genes,quantitative reverse transcription-PCR (QRT-PCR) was carried out for CDC25B and TUSC3 genes,and β-actin gene was taken as internal control.The product of PCR was quantitated by comparative Ct method.RESULTS:The signal of microarray hybridization was clear,and the images had a lower background and higher signal-noise ratio.In comparison with normal pancreas,twenty -four differentially expressed genes were identified which included seventeen up-regulated and seven down-regulated genes.The results of QRT-PCR demonstrated that the expressions of CDC25B and TUSC3 in pancreatic cancer were up-regulated and down-regulated respectively,which is consistent with microarray results.CONCLUSION:The oligonucleotide microarray specialized for pancreatic cancer is desirable for its specialty and sensitivity,which can simultaneously and parallelly detect multiple pancreatic cancer-associated genes.

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