Objective To investigate the expression of E26 transformation-specific-1（E26ts-1），matrix metalloproteinase-1（MMP-1）and tissue inhibitor of matrix metalloproteinase-1 （TIMP-1） in choroidal melanoma and the correlation with the tumorprime;s infiltration and metastasis. Methods Immunohistochemistry was used to detect the expression of E26ts-1，MMP-1 and TIMP-1 in 78 cases of choroidal melanoma who were divided into shuttle-cells，paraepithelial-cells and mixed-cells type according to the configuration of tumor cells.The patients were followed up and their average existing time was calculated.The results were statistically computed with statistic SPSS 10.0 package. Results In the 78 cases，shuttle-cells type was found in 21，paraepithelial-cells type in 34，and mixed-cells type in 23. Expression of TIMP-1was low in uveal melanoma，while expression of E26ts-1 and MMP-1 was obviously found in the three types of choroidal melanoma;the sequence of expression intensity was shuttle-cells，mixed-cells and paraepithelial-cells type.Among 37 cases who had been followed up，the shuttle-cells type was in 18 with the average existing time of （78.33plusmn;24.69）months，the mixed-cells type was in 10 with the average existing time of（61.44plusmn;20.46）months，and the paraepithelial-cells type was in 9 with the average existing time of（36.76plusmn;12.19）months.The existing time was negative correlated with the intensity of expresion of E26ts-1 and MMP-1. Conclusion The high expression of E26ts-1 and MMP-1and low expression of TIMP-1may relate to the choroidal melanomaprime;s infiltration and metastasis. (Chin J Ocul Fundus Dis, 2006, 22: 174-176)
Objective To investigate the inhibitive effect of E2F decoy oligodeoxynucleotides (E2F decoy ODNs) on cultured human retinal pigment epithelial (HRPE) cells.Methods E2F decoy ODNs or scramble decoy ODNs at varied concentrations were put into the HRPE cells mediated by lipofectamineTM2000. The proliferative activity of HRPE was detected by methythiazolyl-terazollium assay, and the competitive combinative activity of E2F decoy ODNs and transcription factor E2F was detected by electrophoresis mobility-shift assay. Results The proliferation of HRPE was inhibited markedly by E2F decoy ODNs at the concentration of 0.2 μmol/L (P=0.002) in a dose-dependent manner but not by scrambled decoy. The results of electrophoresis mobility-shift assay showed that the combinative activity of transcription factor E2F was abolished completely by E2F decoy ODNs. Conclusions E2F decoy ODNs may sequence-specifically inhibit the combinative activity of transcripti on factor E2F,and inhibit the proliferation of HRPE cells.(Chin J Ocul Fundus Dis，2004，20：182-185)
ObjectiveTo investigate the key long non-coding RNAs (lncRNAs) and transcription factors (TFs) in idiopathic pulmonary fibrosis (IPF) by Bioinformatics analysis.MethodsBioinformatics analysis of three gene expression profiles from the Gene Expression Omnibus dataset (GSE2052, GSE44723, and GSE24206), including 42 IPF and 21 normal lung tissues, was performed in this study. Subsequently, differentially expressed genes (DEGs) were filtered, and key genes involved in signaling pathways and the DEG-associated protein-protein interaction network (PPI) were further analyzed. The filtered genes expression was determined by real-time quantitative polymerase chain reaction analysis.ResultsA total of 8483 aberrantly expressed genes were screened, and 29 overlapping genes were identified among these three datasets. A significant enrichment analysis of DEG-associated functions and pathways was further performed. A total of 18 modules were obtained from the DEG PPI network, and most of the modules were involved in polyubiquitination, Golgi vesicle transport, endocytosis and so on. The key genes were obtained through hypergeometric testing, and most of the corresponding genes were closely associated with ubiquitin-mediated proteolysis, the spliceosome, and the cell cycle. These differential expressed genes, such as lncMALAT1, E2F1 and YBX1, were detected in the peripheral blood of IPF patients when compared with those normal control subjects.ConclusionlncMALAT1, E2F1 and YBX1 might be possible regulators for the pathogenesis of idiopathic pulmonary fibrosis.