Project description:To understanding the miRNA expression profiling of cancer stem cells of laryngeal squamous carcinoma, the total RNA of CD133+CD44+ laryngeal cancer stem cells (isolated from LSCC cell line TU-177, named TDP), CD133-CD44- cells (TDN) and parental TU-177 (unsorted TU-177 cells, named TPT) was extracted, followed by miRNA sequencing. Differentially expressed miRNAs were identified.
Project description:To understand the gene expression profiling of cancer stem cells of laryngeal squamous carcinoma, the total RNA of CD133+CD44+ laryngeal cancer stem cells (isolated from LSCC cell line TU-177, named TDP), CD133-CD44- cells (TDN) and parental TU-177 (unsorted TU-177 cells, named TPT) was extracted, followed by RNA sequencing. Differentially expression of lncRNA, mRNA, and circRNA was identified.
Project description:To understand 4-TU labelling kinetics in a novel zebrafish transgenic line (lf:UPRT), we exposed adult lf:UPRT zebrafish (whereby animals have hepatocyte-specific uracil phosphoribosyltransferase expression) with 4-TU for 1, 3, 6 and 9 hours. We then dissected adult livers for SLAM-ITseq to determine the optimal 4-TU labelling time in our SLAM-ITseq workflow to allow us to study hepatocyte-specific nascent transcriptional changes.
Project description:Background: In hepatocellular carcinoma (HCC) genes predictive of survival have been found in both adjacent normal (AN) and tumor (TU) tissues. The relationships between these two sets of predictive genes and the general process of tumorigenesis and disease progression remains unclear Methodology/Principal Findings: Here we have investigated HCC tumorigenesis by comparing gene expression (GSE25097), DNA copy number variation and survival using ~250 AN and TU samples representing, respectively, the pre-cancer state, and the result of tumorigenesis. Genes that participate in tumorigenesis were defined using a gene-gene correlation meta-analysis procedure that compared AN versus TU tissues. Genes predictive of survival in AN (AN-survival genes) were found to be enriched in the differential gene-gene correlation gene set indicating that they directly participate in the process of tumorigenesis. Additionally the AN-survival genes were mostly not predictive after tumorigenesis in TU tissue and this transition was associated with and could largely be explained by the effect of somatic DNA copy number variation (sCNV) in cis and in trans. The data was consistent with the variance of AN-survival genes being rate-limiting steps in tumorigenesis and this was confirmed using a treatment that promotes HCC tumorigenesis that selectively altered AN-survival genes and genes differentially correlated between AN and TU. Conclusions/Significance: This suggests that the process of tumor evolution involves rate-limiting steps related to the background from which the tumor evolved where these were frequently predictive of clinical outcome. Additionally treatments that alter the likelihood of tumorigenesis occurring may act by altering AN-survival genes, suggesting that the process can be manipulated. Further sCNV explains a substantial fraction of tumor specific expression and may therefore be a causal driver of tumor evolution in HCC and perhaps many solid tumor types
Project description:Neural-specific mRNA decay measurements by TU-Decay technique in control and Pumilio knockdown embryos These TU-Decay microarrays analyze mRNA levels at three timepoints: a one hour pulse, one hour chase, and three hour chase. Neural-specific RNA purification was achieved using prospero-GAL4 driving UAS-T.g.UPRT. Pumilio knockdown in the nervous system was acheived using UAS-Pum(RNAi) driven by prospero-Gal4.
