Project description:H2AX has been characterized as a novel tumor suppressor protein. Difficiency of H2AX will result in apoptotic inhibition of cancer cells. However, how H2AX epigenetically regulates apoptosis of cancer cells is still unclear To reveal the miRNA expression regulated by H2AX and involved in apoptosis, the microarray profiling analysis was employed to identify differentially expressed miRNAs in H2AX knockdown lung cancer cells and control ones after apoptotic induction. H2AX was knockdown by miRNA interfering system in human lung cancer originated cell A549 and the stable cell line named P1, while the control stable cell line named C. Genes with greater than 1.5-fold change and P-value <0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction.
Project description:H2AX has been characterized as a novel tumor suppressor protein. Difficiency of H2AX will result in apoptotic inhibition of cancer cells. However, how H2AX epigenetically regulates apoptosis of cancer cells is still unclear To reveal the miRNA expression regulated by H2AX and involved in apoptosis, the microarray profiling analysis was employed to identify differentially expressed miRNAs in H2AX knockdown lung cancer cells and control ones after apoptotic induction. H2AX was knockdown by miRNA interfering system in human lung cancer originated cell A549 and the stable cell line named P1, while the control stable cell line named C. Genes with greater than 1.5-fold change and P-value ?0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction. The two groups including control (C) and H2AX knockdown lung cancer cells (P1) were harvested 48 h after VP-16 treatment. Three independent experiments were performed for each group.
Project description:H2AX has been characterized as a novel tumor suppressor protein. Difficiency of H2AX will result in apoptotic inhibition of cancer cells. However, how H2AX epigenetically regulates apoptosis of cancer cells is still unclear. To reveal the genes expression regulated by H2AX and involved in apoptosis, the microarray profiling analysis was employed to identify differentially expressed genes in H2AX knockdown lung cancer cells and control ones after apoptotic induction. H2AX was knockdown by miRNA interfering system in human lung cancer originated cell A549 and the stable cell line named P1, while the control stable cell line named C. Genes with greater than 1.2-fold change and P-value <0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction.
Project description:H2AX has been characterized as a novel tumor suppressor protein. Difficiency of H2AX will result in apoptotic inhibition of cancer cells. However, how H2AX epigenetically regulates apoptosis of cancer cells is still unclear. To reveal the genes expression regulated by H2AX and involved in apoptosis, the microarray profiling analysis was employed to identify differentially expressed genes in H2AX knockdown lung cancer cells and control ones after apoptotic induction. H2AX was knockdown by miRNA interfering system in human lung cancer originated cell A549 and the stable cell line named P1, while the control stable cell line named C. Genes with greater than 1.2-fold change and P-value ï¼0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction. The two groups including control (C) and H2AX knockdown lung cancer cells (P1) were harvested 48 h after VP-16 treatment. Three independent experiments were performed for each group.
Project description:We have sequenced miRNA libraries from human embryonic, neural and foetal mesenchymal stem cells. We report that the majority of miRNA genes encode mature isomers that vary in size by one or more bases at the 3’ and/or 5’ end of the miRNA. Northern blotting for individual miRNAs showed that the proportions of isomiRs expressed by a single miRNA gene often differ between cell and tissue types. IsomiRs were readily co-immunoprecipitated with Argonaute proteins in vivo and were active in luciferase assays, indicating that they are functional. Bioinformatics analysis predicts substantial differences in targeting between miRNAs with minor 5’ differences and in support of this we report that a 5’ isomiR-9-1 gained the ability to inhibit the expression of DNMT3B and NCAM2 but lost the ability to inhibit CDH1 in vitro. This result was confirmed by the use of isomiR-specific sponges. Our analysis of the miRGator database indicates that a small percentage of human miRNA genes express isomiRs as the dominant transcript in certain cell types and analysis of miRBase shows that 5’ isomiRs have replaced canonical miRNAs many times during evolution. This strongly indicates that isomiRs are of functional importance and have contributed to the evolution of miRNA genes