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Chidamide inhibits the NOTCH1-MYC signaling axis in T-cell acute lymphoblastic leukemia

ABSTRACT: Chidamide inhibits the NOTCH1-MYC signaling axis in T-cell acute lymphoblastic leukemia

PROVIDER: PRJNA672977 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12926480_1.fastq.gz	Fastqsanger.gz
	SRR12926480_2.fastq.gz	Fastqsanger.gz
	SRR12926481_1.fastq.gz	Fastqsanger.gz
	SRR12926481_2.fastq.gz	Fastqsanger.gz
	SRR12926482_1.fastq.gz	Fastqsanger.gz

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Chidamide inhibits the NOTCH1-MYC signaling axis in T-cell acute lymphoblastic leukemia

Project description:We report that Chidamide shows significant anti- proliferation and more specifically anti-NOTCH effects in both cell lines and primary cells of T-ALL patients. By analyzing the expression profile characterizing the response of the cell lines to Chidamide treatment, we further confirmed that the antitumor effect of Chidamide was due to the inhibition of HDAC and the anti-NOTCH1 effect.

2021-12-31 | GSE160349 | GEO

Chidamide inhibits double expressor lymphoma through repressing Myc expression and activity

Project description:Double-expressor lymphoma (DEL), defined by MYC and BCL-2 overexpression without corresponding chromosome translocations, is often associated with poor outcomes for standard treatment (R-CHOP). Recently, inhibitors of histone deacetylases have shown great effect in T cell lymphomas. However, its effects on B cell lymphomas are mild. Here, our clinical retrospective analysis showed that HDAC inhibitor chidamide combined with R-CHOP (CR-CHOP) can dramatically increase the complete remission rate of patients with DEL. And the sensitivity of B cell lymphoma cell lines to chidamide is negatively correlated to Myc level. From Western blots and transcriptomics analysis, we found that chidamide treatment could reduce Myc protein level and downregulate the transcription levels of corresponding Myc downstream targets. Thus our results indicate that HDAC inhibitor chidamde holds great potential for treating DEL, which likely functions through inhibiting the Myc pathway.

2022-04-24 | GSE173285 | GEO

Chidamide inhibits double expressor lymphoma through repressing Myc expression and activity

Project description:Chidamide inhibits double expressor lymphoma through repressing Myc expression and activity

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Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling

Project description:Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling

| PRJNA1209364 | ENA

RUNX1 colludes with NOTCH1 to reprogram chromatin in T cell acute lymphoblastic leukemia

Project description:Runt-related transcription factor 1 (RUNX1) is oncogenic in diverse types of leukemia and epithelial cancers where its expression is associated with poor prognosis. Current models suggest that RUNX1 cooperates with other oncogenic factors (e.g., NOTCH1, TAL1) to drive the expression of proto-oncogenes in T cell acute lymphoblastic leukemia (T-ALL) but the molecular mechanisms controlled by RUNX1 and its cooperation with other factors remain unclear. Integrative chromatin and transcriptional analysis following inhibition of RUNX1 and NOTCH1 revealed a surprisingly widespread role of RUNX1 in the establishment of global H3K27ac levels and that RUNX1 is required by NOTCH1 for cooperative transcription activation of key NOTCH1 target genes including MYC, DTX1, HES4, IL7R, and NOTCH3. Super-enhancers were preferentially sensitive to RUNX1 knockdown and RUNX1-dependent super-enhancers were disrupted following the treatment of a pan-BET inhibitor, I-BET151.

2023-03-26 | GSE99705 | GEO

RUNX1 colludes with NOTCH1 to reprogram chromatin in T cell acute lymphoblastic leukemia

2023-03-26 | GSE99704 | GEO

RUNX1 colludes with NOTCH1 to reprogram chromatin in T-cell acute lymphoblastic leukemia

2023-03-25 | GSE99706 | GEO

Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling [ChIP-Seq]

Project description:Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling [ChIP-Seq]

| PRJNA1211995 | ENA

Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling [ATAC-Seq]

Project description:Endothelial KLF15/VASN axis inhibits angiogenesis via activation of Notch1 signaling [ATAC-Seq]

| PRJNA1212002 | ENA

Therapeutic targeting of the NOTCH1 and neddylation pathways in T cell acute lymphoblastic leukemia

Project description:Gamma Secretase Inhibitors (GSIs) effectively block the activation of oncogenic protein Notch homolog-1 (NOTCH1), a frequent event in T-cell Acute Lymphoblastic Leukemia (T-ALL). However, their clinical application is hampered by severe gastrointestinal toxicity due to the inhibition of NOTCH1 signaling and subsequent increase in goblet cell differentiation in the gut. Genome-wide CRISPR loss-of-function (LOF) screen in the colon cancer cell line LS174T identified the neddylation pathway as a main regulator of goblet cell differentiation upon NOTCH1 inhibition. Consistently, genetic deletion or pharmacologic inhibition of the neddylation pathway with the small molecule inhibitor MLN4924 rescued GSI-induced differentiation and cell death in LS174T cells. Mechanistically, neddylation inhibition by MLN4924 increases the protein stability of Hairy and enhancer of split-1 (HES1), a known NOTCH1 target and a regulator of absorptive and secretory cell fate decisions. Combined treatment with GSI and MLN4924 in murine Notch1-induced model of T-ALL showed leukemia regression and improved overall survival without any associated gut toxicity. Overall, these results substantiate the potential of targeting NOTCH1 and neddylation pathway in the treatment of NOTCH1-induced T-ALL. We used microarray to profile the gene expression in mouse intestinal stem cells upon NOTCH1 inhibition through GSI (DBZ treatment). This will allow us to explore the mechanisms of NOTCH1 inhibition in intestinal cell fate in vivo.

2025-04-01 | GSE245370 | GEO

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