Project description:We performed ChIP-seq to compare genome-wide HIF-1b and HIF-2a occupancy in wild type 786-O cells to 786-O cells with either HIF-1b or HIF-2a endogenously tagged with a V5-Halo moiety.
Project description:We performed RNA-Seq analysis of wildtype and three EPAS1-/- 786-O single cell clones generated by CRISPR/Cas9 to identify the HIF-2a-responsive genes in this cell line. Samples from wildtype 786-O cells treated with DMSO or HIF-2a antagonist compound C2 were also included in this analysis.
Project description:In order to determine how NAT10 regulates NFE2L3 to promote the progression of ccRCC, since NFE2L3 is a transcription factor, we performed CHP-seq detection for NFE2L3, as well as RNA-seq detection for 786-O cells with stable NFE2L3 knocking and control 786-O cells. The results of RNA-seq showed that 312 transcripts in the NFE2L3 knockdown group were down-regulated, and 3 114 transcripts in the previous ccRCC tissue were up-regulated. Moreover, after comprehensive analysis of ChIP-seq, there were 12 overlapping transcripts. Analysis of the expression levels of 12 transcripts in control cells and stable NFE2L3 knockout cells showed that the expression level of LASP1 was the highest in cells, so we hypothesized that NFE2L3 promoted the progression of ccRCC by affecting LASP1.
Project description:RNA-seq analysis were applied to elucidate the transcriptional differences between 786-O cell lines transfected with control-sgRNA (Control) and PHF8-sgRNA (PHF8-KO). A total of 3575 differentially expressed genes (Fold Change > 2, or Fold Change<0.5; FDR < 0.05) with 2097 down- and 1478 up-regulated genes were identified in PHF8-KO 786-O cells
Project description:VHL loss is the most common genetic alteration event in ccRCC. We profiled histone modifications from VHL-deficient ccRCC primary tumors and cell lines. We show that ccRCCs exhibit a pervasive gain of enhancers around hypoxic and metabolic transcriptional targets. Motif analysis using HOMER revealed significant enrichment of AP-1, ETS, NFĸB and HIFα in tumor enhancers. We generated ChIP-seq binding data for c-Jun, ETS1, NFĸB, and P300, a histone acetyltransferase, in 786-O cells. ChIP-seq profiles of HIF2α and HIF1β in 786-O were already generated previously (GSE34871)
Project description:To explore the signaling network involving circDVL1, miR-412-3p, and its targets in ccRCC, we used RNA sequencing (RNA-seq) to identify potential miR-412-3p target genes in miR-412-3p overexpressing and control cells. RNA-seq data identified 392 mRNAs that were downregulated in miR-412-3p overexpressing 786-O cells
Project description:In order to determine how NAT10 regulates NFE2L3 to promote the progression of ccRCC, since NFE2L3 is a transcription factor, we performed CHP-seq detection for NFE2L3, as well as RNA-seq detection for 786-O cells with stable NFE2L3 knocking and control 786-O cells. The results of RNA-seq showed that 312 transcripts in the NFE2L3 knockdown group were down-regulated, and 3 114 transcripts in the previous ccRCC tissue were up-regulated. Moreover, after comprehensive analysis of ChIP-seq, there were 12 overlapping transcripts. Analysis of the expression levels of 12 transcripts in control cells and stable NFE2L3 knockout cells showed that the expression level of LASP1 was the highest in cells, so we hypothesized that NFE2L3 promoted the progression of ccRCC by affecting LASP1.
Project description:We have used in vivo selection to isolate GPX4 knockout 786-O cells that have evaded ferroptosis in vivo in mouse xenograft experiments. RNA-seq and Exome-seq profiling were performed to characterize the mechanisms underlying ferroptosis evasion in these in vivo-derived ferroptosis resistant cells.