Project description:Deubiquitinating enzymes (DUBs) are divided into seven subgroups based on sequence and structure and perform the roles of mediating the deubiquitination of substrate proteins, regulating protein function, and participating in various cellular life activities. Among them, the ubiquitin-specific protease family (USP) is the DUB subtype with the most members and structural diversity discovered so far. USP48 is a member of the USP family of ubiquitin-specific proteases and has been found to promote glioblastoma by deubiquitinating the Gli1 transcription factor and to promote the progression of non-small-cell lung cancer through inhibition of the Wnt/β-catenin signaling pathway. We used microarrays to detail changes in gene expression regulated by USP48 overexpression in HCC cells.
Project description:RNA transcriptome sequencing analysis was performed in SNU-668 Erastin-resistant cells and SNU-668 parental cells, SNU-484 RSL3-resistant cells and SNU-484 parental cells
Project description:Purpose: The goal of this experiment is to investigate the relative contributions of various types of cell death in NaIO3-treated RPE cells Methods: RPE cell mRNA profiles were generated by deep sequencing, in triplicate, using Illumina HiSeq 4000. Results: According to the differential expressions of mRNA genes, among which 661 genes were upregulated and 637 genes were downregulated with significance after NaIO3 treatment . From the Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, it has been identified that ferroptosis ranked as the top pathway in comparison to other types of cell death (apoptosis, and necroptosis) upon NaIO3 treatment, which was additionally validated by the higher FPKM of main regulators in ferroptosis than that in apoptosis. Additionally, it was found that heme oxygenase-1 (HMOX1, also known as HO-1) as well as SLC7A11 (solute carrier family 7 member 11) mRNA were characterized as the most dramatically upregulated genes upon NaIO3 treatment against ARPE-19 cells Conclusions: Our study represented that ferroptosis serves as a predominant pathogenic factor involved in AMD pathological process.
Project description:purpose:To compare the enrichment of H3K27me3 on genes after treatment of control and α-KG. Method: Primary cardiomyocytes were treated with control (PBS) and α-KG for 24 h and precipitated with H3K27me3 antibody, then, the precipitated sequences were analysed by next generation RNA-seq. Results: There are significant differences between control and α-KG group. Conclusion:H3K27me3 ChIP-seq was used for analysing the enrichment of H3K27me3 on genes.
Project description:Purpose: The goals of this study are to compare the gene expression profile of Huh7 cells treated with different ectosomes or not and to evaluate the function of ectosomal Hexokianse 1 (HK1) derived from HSCs. Methods: Firstly, we treated different LX-2 HSCs with TGF-β (2 ng/mL) for 36 hours to activate HSCs, then ectosomes from LX-2 or HK1-KD LX-2 culture medium were isolated respectively by differential centrifugation processes. Secendly, Huh7 cells were preincubated with different ectosomes or not for 12 hours and then fresh medium for another 12 hours. Lastly, different groups of Huh7 cells were prepared for RNA-seq. Results: By Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of the differentially expressed genes, a total of 124 pathways were found to be enriched in the ectosome-incubated Huh7 cells compared with the control Huh7 cells, while a total of 36 pathways were enriched in the ectosome-incubated Huh7 cells compared with the HK1-KD ectosome-incubated Huh7 cells.Gene set enrichment analysis (GSEA) also revealed enrichment of the N-glycosylation pathway in the ectosome-incubated Huh7 cells compared with the control Huh7 cells. Conversely, this pathway was negatively regulated in Huh7 cells incubated with HK1-KD HSC-derived ectosomes Conclusion: the transferal of HSC-derived ectosomal HK1 into HCC cells regulates the N-glycosylation level of Huh7.