Objective　To evaluate the correlation between vascular endothelial growth factor(VEGF) expression and microvessel density(MVD) in gastric carcinoma (GC) and the relationship of VEGF and MVD with clinicopathologic characteristics and prognosis of GC. Methods　The expression of VEGF and intratumoral microvessel density (MVD) in one hundred and sixteen resected specimens of the patients with GC were observed and counted, and the relationship of VEGF and MVD with clinicopathologic factors and prognosis of GC were analysed. Results　The expression of VEGF was found in 60.34% of the specimens. The MVD value was much higher in VEGF(+) group than that in VEGF(-) group (26.16±8.50 and 19.22±8.20, respectively, P<0.01). Expression of VEGF was significantly higher in patients with lymph node metastasis than that in patients without lymph node metastasis (p<0.05).Expression of VEGF was highly correlated with the stage of tumor (P<0.05). MVD correlated with lymph node metastasis (P<0.01) and abdomen metastasis (P<0.01) and increased with the TNM stage (P<0.01). The total five-year survival rate in VEGF(-) group and low MVD group were significantly higher than that in VEGF(+) group and high MVD group respectively(both P<0.01). Multivariate analysis indicated that the expression of VEGF and MVD were independent prognostic factors of GC. Conclusions　The expression of VEGF and MVD can reflect the malignant degree of GC. They may serve as the prognostic factors and guide the decisions on the therapy.

OBJECTIVETo investigate the effects of siRNAs targeting CD97 immune epitopes on proliferation, infiltration, apoptosis and cell cycle of breast cancer cells.

METHODSsiRNA sequences targeting CD97and CD97immune epitopes were designed according to Gene Bank NM_001025160.2 with smart siCatchsiRNA design software. CD97siRNAs were transfected into MDA-MB231 cells in which CD97 was highly expressed. Highest sensitive CD97and CD97siRNA were screened by Western blotting. Inverted microscope was used to observe the growth of CD97siRNAs-transfected MDA-MB231 cells; the proliferation activity of MDA-MB231 cells was detected by MTT method; the wound healing assay and Transwell migration test were performed to examine the migration and infiltration ability of CD97and CD97siRNA-transfected MDA-MB231 cells; the effects of CD97siRNA and CD97siRNA on cell apoptosis and cell cycle of MDA-MB231 cells were detected by TUNEL and flow cytometry.

RESULTSThe growth and proliferation activity of CD97siRNAs-transfected MDA-MB231 cells were significantly lower than those in the control groups, and such differences were more significant in CD97siRNA-transfected group (all<0.05); scratch test showed that the wound healing rate was lower in CD97siRNAs-transfected groups, especially in CD97siRNA-transfected group (all<0.05); Transwell migration showed that the number of MDA-MB231 cells crossing through chambers were less in CD97siRNAs-transfected groups, especially in CD97siRNA-transfected group (all<0.05); no significant difference in cell apoptosis was observed between CD97siRNAs-transfected groups and control groups; cell cycle detection showed that CD97siRNAs-transfected groups had less cells in G/Gphase and more cells in S phase compared with the control groups, and such effect on cell cycle was more marked in CD97siRNA-transfected group (all<0.05).

CONCLUSIONSCD97 plays an important role in the cell growth, proliferation, migration and invasion of breast cancer MDA-MB231 cells, and compared with CD97, CD97may have more effective inhibitory effects on cellular malignant behaviors.

Primitive mammalian heart transforms from a single tube to a four-chambered muscular organ during a short developmental window. We found that knocking out global microRNA by deleting Dgcr8 microprocessor in Mesp1 cardiovascular progenitor cells lead to the formation of extremely dilated and enlarged heart due to defective cardiomyocyte (CM) differentiation. Transcriptome analysis revealed unusual upregulation of vascular gene expression in Dgcr8 cKO hearts. Single cell RNA sequencing study further confirmed the increase of angiogenesis genes in single Dgcr8 cKO CM. We also performed global microRNA profiling of E9.5 heart for the first time, and identified that miR-541 was transiently highly expressed in E9.5 hearts. Interestingly, introducing miR-541 back into microRNA-free CMs partially rescued their defects, downregulated angiogenesis genes and significantly upregulated cardiac genes. Moreover, miR-541 can target Ctgf and inhibit endothelial function. Our results suggest that microRNAs are required to suppress abnormal angiogenesis gene program to maintain CM differentiation.