ABSTRACT
Objective To investigate the expression of Sema4 D and Ki67 in pancreatic carcinoma and its relationship with clinicopathological features. Methods The expression of Sema4 D and Ki67 in 40 pancreatic carcinoma tissues and 10 adjacent tissues was measured by immunohistochemistry, and its relationship with the clinicopathological features of pancreatic carcinoma was analyzed. Comparison of categorical data between two groups was made by chi-square test. Spearman's rank correlation analysis was used to identify the correlation between these variables. Results Sema4 D and Ki67 were detected in 19 (47. 5％ ) and 18 (45. 0％ ), respectively, of the 40 pancreatic carcinoma tissues, with significantly higher positive rates than the adjacent tissues (χ2= 10. 040 and 10. 000, P = 0. 020 and 0. 022) . The abnormal expression of Sema4 D and Ki67 differed significantly between patients with different tumor stages and between patients with and without lymph node metastasis (χ2= 6. 352, 4. 912, 12. 031, and 6. 465, P = 0. 013, 0. 028, 0. 001, and 0. 025) . Sema4 D expression was positively correlated with Ki67 expression (r = 0. 347, P = 0. 028) . Conclusion The expression of Sema4 D and Ki67 is elevated in pancreatic carcinoma compared with the adjacent tissue. Their expression is positively correlated with each other and is associated with tumor staging and lymph node metastasis.
ABSTRACT
Objective:To construct a small interfering RNA(siRNA)expression vector(psiRNA-VEGFR-3)targeting vascular endothelial growth factor receptor 3(VEGFR-3)and to investigate the effects of VEGFR-3 siRNA on the adherence and invasion of human colon cancer cells.Methods:A siRNA expression vector(psiRNA-VEGFR-3)targeting VEGFR-3 were constructed and was used to transfect LoVo cells via lipofectamine 2000.The mRNA and protein expression of VEGFR-3 were examined after transfection by reverse transcriptase polymerase chain reaction(RT-PCR)and Western blotting,respectively.The tumor adhesion ability was detected by cell-matrix adhesion experiment and the invasion ability of tumor cells was evaluated by millicell chamber model.Results:The VEGFR-3 siRNA expression vector was successfully constructed.The expression of VEGFR-3 mRNA and protein was inhibited after psiRNA-VEGFR-3 transfection.Seventy-two hours after psiRNA-VEGFR-3 transfection,Western blotting assay showed that the expression of VEGFR-3 protein was decreased from(1.26?0.19)to(0.39 s0.12)(P