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.
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 , GeneticsABSTRACT
<p><b>OBJECTIVES</b>To investigate the trends in incidence and long-term recurrence rate of pilonidal sinus disease (PSD) within the German Armed Forces, and analyse the influence of variable factors, such as different surgical methods, body constitution and smoking amount, to incidence and long-term recurrence rate of PSD.</p><p><b>METHODS</b>Information of all the patients being admitted with primary PSD to the surgical departments of three hospitals of the German Armed Forces between 1980 and 1996 was collected and analyzed, 500 patients of which were interviewed.</p><p><b>RESULTS</b>Two of the 500 patients were dead, and every one of the rest 498 patients agreed to take part in the interview. The incidence of PSD rose from 0.3/1000 in 1985 to 2.4/1000 in 2007. The recurrence rates were decreasing within 16 years of treatment from 33% in 1981 via 23% in 1986 to 12% in 1996 (P = 0.01). Recurrence rates of primary open wound healing (16.8%) compared to primary suture (31.0%) differ significantly (P < 0.01). While the mean body weight within the army rose 1 kg per decade, population shows an increase of 1.9 kg per decade though not being an influencing factor on the recurrence rate (P = 0.72). Smoking of more than 20 cigarettes per day proved to be a significant factor on the recurrence rate of PSD (P = 0.015).</p><p><b>CONCLUSION</b>While the recurrence rates-especially of primary open wound treatment-decreased, the incidence of PSD rose nearly tenfold.</p>