Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenetic and metabolic reprogramming by HDAC inhibition targets NRF2-active tumors [RNA-Seq]

ABSTRACT: To investigate the NRF2-specific cytotoxic effects of HDAC inhibition, we assessed gene expression in the context of control and NRF2-overexpressing mouse LUAD cells upon HDAC inhibition.

ORGANISM(S): Mus musculus

PROVIDER: GSE220837 | GEO | 2023/03/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Epigenetic and metabolic reprogramming by HDAC inhibition targets NRF2-active tumors [CUT&Tag]

Project description:To investigate the NRF2-specific cytotoxic effects of HDAC inhibition, we assessed genomic distribution of histone acetylation modifications and readers in the context of control and NRF2-overexpressing mouse LUAD cells upon HDAC inhibition.

2023-03-30 | GSE220832 | GEO

Epigenetic and metabolic reprogramming by HDAC inhibition targets NRF2-active tumors [CRISPR Screen]

Project description:To identify NRF2-specific dependencies in chromatin regulation, we performed a focused genetic screen mouse LUAD cell lines with or without knock-out of KEAP1.

2023-03-30 | GSE220831 | GEO

Epigenetic and metabolic reprogramming by HDAC inhibition targets NRF2-active tumors

Project description:Epigenetic and metabolic reprogramming by HDAC inhibition targets NRF2-active tumors

| PRJNA911718 | ENA

Epigenetic and metabolic reprogramming by HDAC inhibition targets NRF2-active tumors [CUT&Tag]

Project description:Epigenetic and metabolic reprogramming by HDAC inhibition targets NRF2-active tumors [CUT&Tag]

| PRJNA911637 | ENA

Epigenetic and metabolic reprogramming by HDAC inhibition targets NRF2-active tumors [CRISPR Screen]

Project description:Epigenetic and metabolic reprogramming by HDAC inhibition targets NRF2-active tumors [CRISPR Screen]

| PRJNA911659 | ENA

Epigenetic and metabolic reprogramming by HDAC inhibition targets NRF2-active tumors [RNA-Seq]

Project description:Epigenetic and metabolic reprogramming by HDAC inhibition targets NRF2-active tumors [RNA-Seq]

| PRJNA911727 | ENA

HDAC inhibitors in synovial sarcoma cells

Project description:Histone deacetylase (HDAC) inhibition has been shown in previous studies to disrupt the synovial sarcoma oncoprotein complex, resulting in apoptosis. To understand the molecular effects of HDAC inhibition, RNA-Seq transcriptome analysis was undertaken in six human synovial sarcoma cell lines. HDAC inhibition induced pathways of cell cycle arrest, neuronal differentiation and response to oxygen-containing species, effects also observed in other cancers treated with this class of drugs. More specific to synovial sarcoma, polycomb-group targets were reactivated including tumor suppressor CDKN2A, and pro-apoptotic transcriptional patterns were induced. Functional analyses revealed that ROS-mediated FOXO activation and pro-apoptotic factors BIK, BIM and BMF were important to apoptosis induction following HDAC-inhibition in synovial sarcoma

| EGAS00001002637 | EGA

Transcriptional profiling of BL/6 mice with alterations in Kras, Stk11, and/or Keap1/Nrf2.

Project description:Transcriptional profiling of BL/6 mice harboring a mutant Kras allele, with or without knockouts of Stk11 and/or Keap1, or with expression of an Nfe2l2 transgene, Nrf2Tg. In lung adenocarcinoma (LUAD), stabilization of the transcription factor NRF2 through genomic alterations in KEAP1 and NFE2L2 occurs in roughly a quarter of patients, often in the context of STK11 tumor suppressor loss. In this study, we demonstrate that NRF2 activation in the context of concurrent KRAS mutation and STK11 loss promotes aggressive LUAD tumor behavior in both human and mouse preclinical models. This phenotype is associated with metabolic rewiring and rescue by NRF2 of redox stress, high in STK11 null tumors. Applying a novel, pan-lung cancer, diagnostic NRF2 activation gene expression signature that is independent of frequently co-occurring mutations, we dissect the independent contributions of the three most frequent genetic events in human LUAD (NRF2 activation, STK11 loss and KRAS mutations) on patient prognosis and clinical responses in a dataset of second-line LUAD patients treated with immunotherapy or chemotherapy (OAK trial). Our findings underscore that both individual effects and epistatic relationships among oncogenic and tumor suppressor pathways influence tumor biology, immune contexture and patient clinical outcomes. Our work also highlights the value of lung cancer disease sub-classification based on genetic and expression profiling as part of patient clinical management.

2020-01-31 | GSE133714 | GEO

Epigenetic and metabolic reprogramming by HDAC inhibition targets NRF2-active tumors

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-03-30 | GSE220839 | GEO

Nrf2 transcript alterations

Project description:WGS and RNA-seq data for Nrf2 study

| EGAS00001001740 | EGA