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NAT10 promotes the progression of clear cell renal cell carcinoma by regulating ac4C acetylation of NFE2L3 and activating AKT/GSK3β signaling pathway [RNA-seq]

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE226941 | GEO | 2023/03/18

REPOSITORIES: GEO

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NAT10 promotes the progression of clear cell renal cell carcinoma by regulating ac4C acetylation of NFE2L3 and activating AKT/GSK3β signaling pathway [ChIP-seq]

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.

2023-03-18 | GSE226940 | GEO

NAT10 promotes the progression of clear cell renal cell carcinoma by regulating ac4C acetylation of NFE2L3 and activating AKT/GSK3β signaling pathway

Project description:To determine the role of NAT10 in promoting the progression of ccRCC, we performed RNA sequencing (RNA-Seq) and ac4C-modified RNA immunoprecipitation sequencing (acRIP-seq) on four pairs of ccRCC tissues and their adjacent tissues. A comprehensive analysis of acRIP-seq and RNA-seq showed that the expression and acetylation levels of 199 transcripts were increased . We selected 11 candidate genes of interest and analyzed their acetylation levels. Since ac4C modification can improve mRNA stability, the 11 candidate genes were verified, and the results showed that only NFE2L3 mRNA levels decreased in 786-O cells and A498 cells after NAT10 stable knockdown , so we decided to study the mechanism of action of NFE2L3 in ccRCC.

2023-03-18 | GSE226863 | GEO

Nfe2l3 promotes neuroprotection and long-distance axon regeneration after injury in vivo [bulkRNA-seq]

Project description:Nuclear factor erythroid 2 like (Nfe2l) gene family members 1-3 mediate cellular response to oxidative stress, including in the central nervous system (CNS). However, neuronal functions of Nfe2l3 are unknown. Here, we comparatively evaluated expression of Nfe2l1, Nfe2l2, and Nfe2l3 in singe cell RNA-seq (scRNA-seq)-profiled cortical and retinal ganglion cell (RGC) CNS projection neurons, investigated whether Nfe2l3 regulates neuroprotection and axon regeneration after CNS injury in vivo, and characterized a gene network associated with Nfe2l3 in neurons. We showed that, Nfe2l3 expression transiently peaks in developing immature cortical and RGC projection neurons, but is nearly abolished in adult neurons and is not upregulated after injury. Furthermore, within the retina, Nfe2l3 is enriched in RGCs, whereas Nfe2l1 and Nfe2l2 are expressed robustly in other retinal cell types as well, and are also upregulated after injury. We also found that, expressing Nfe2l3 in injured RGCs through localized intralocular viral vector delivery promotes neuroprotection and long-distance axon regeneration after optic nerve injury in vivo. Moreover, Nfe2l3 treatment provided a similar extent of neuroprotection and axon regeneration as viral vector-targeting of Pten and Klf9, which are prominent regulators of neuroprotection and long-distance axon regeneration. Finally, we bioinformatically characterized a gene network associated with Nfe2l3 in neurons, which revealed the association of Nfe2l3 with established mechanisms of neuroprotection and axon regeneration. Thus, Nfe2l3 is a novel neuroprotection and axon regeneration-promoting factor with a therapeutic potential for treating CNS injury and disease.

2024-02-22 | GSE253838 | GEO

Nfe2l3 promotes neuroprotection and long-distance axon regeneration after injury in vivo [Third party: scRNA-seq]

2024-02-22 | GSE253839 | GEO

NFE2L3 Drives Hepatocellular Carcinoma Proliferation via Regulating the Proteasome-Dependent Degradation of ISGylation p53 through interaction with TRIM25.

Project description:To investigate the function of NFE2L3 and NFE2L3△C(557-694aa) in the regulation of hepatocellular carcinoma proliferation, we established HepG2 cell lines in which the target gene has been over express by lentiviruses. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different cells at three-time points.

2023-09-13 | GSE210803 | GEO

Transcription factors enriched in tumor-associated enhancers in VHL-deficient ccRCC

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)

2017-08-22 | GSE86092 | GEO

Overexpression of Parkin in clear cell renal cell carcinoma decreases tumor aggressiveness by regulating CKS2 levels

Project description:Here we analyzed ccRCC 786-O cells with overexpressed Parkin in contrast to wild type and control cells. While differences between 786-O wild type and control cells were rather moderate, quite some differences were found between 786-O wild type/control cells and cells overexpressed with Parkin.

2022-02-16 | PXD029398 | Pride

Expression data from 786-O renal cell cancer cells treated with pentamidine

Project description:While early stages of clear cell renal cell carcinoma (ccRCC) are curable, survival outcome for metastatic ccRCC remains poor. The purpose of the current study was to apply a new individualized bioinformatics analysis (IBA) strategy to these transcriptome data in conjunction with Gene Set Enrichment Analysis of the Connectivity Map (C-MAP) database to identify and reposition FDA-approved drugs for anti-cancer therapy. We demonstrated that one of the drugs predicted to revert the RCC gene signature towards normal kidney, pentamidine, is effective against RCC cells in culture and in a RCC xenograft model. Most importantly, pentamidine slows tumor growth in the 786-O human ccRCC xenograft mouse model. To determine which genes are regulated by pentamidine in a human RCC cell line, 786-O, we treated these cells with pentamidine and performed transcriptional profiling analysis. We used microarrays to determine the set of genes regulated by pentamidine in 786-O renal cell cancer cells. Total RNA was isolated from 786-O cells treated with 25 Î¼M pentamidine or vehicle control (DMSO) for 6 hours and hybridized to Affymetrix microarrays.

2014-08-05 | E-GEOD-54709 | biostudies-arrayexpress

ZDHHC2-mediated AGK S-palmitoylation inactivates PTEN to reduce sensitivity to sunitinib in ccRCC

Project description:To investigate the role of ZDHHC2 in regulating the sensitivity of ccRCC to TKIs, we established 786-O cell lines in which each target gene has been knocked down by siRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq.

2022-05-24 | GSE203485 | GEO

Systematic Analysis of Transcriptomic Profile of Renal Cell Carcinoma under Long-Term Hypoxia using Next-Generation Sequencing and Bioinformatics

Project description:Patients with clear cell renal cell carcinoma (ccRCC) are often diagnosed with both von Hippel-Lindau (VHL) mutations and the constitutive activation of hypoxia-inducible factor-dependent signaling. In this study, we investigated the effects of long-term hypoxia in 786-O, a VHL-defective renal cell carcinoma cell line, to identify potential genes and microRNAs associated with tumor malignancy. The transcriptomic profiles of 786-O under normoxia, short-term hypoxia, and long-term hypoxia were analyzed using next-generation sequencing. The results showed that long-term hypoxia promoted the ability of colony formation and transwell migration compared to normoxia. In addition, the differentially expressed genes induced by long-term hypoxia were involved in various biological processes including cell proliferation, the tumor necrosis factor signaling pathway, basal cell carcinoma, and cancer pathways. The upregulated (L1CAM and FBN1) and downregulated (AUTS2, MAPT, AGT, and USH1C) genes in 786-O under long-term hypoxia were also observed in clinical ccRCC samples along with malignant grade. The expressions of these genes were significantly correlated with survival outcomes in patients with renal cancer. We also found that long-term hypoxia in 786-O resulted in decreased expressions of hsa-miR-100 and has-miR-378, and this effect was also observed in samples of metastatic ccRCC compared to samples of non-metastatic ccRCC. These findings may provide a new direction for the study of potential molecular mechanisms associated with the progression of ccRCC.

2017-12-12 | GSE107848 | GEO

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