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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.

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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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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.

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

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

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Expression data from c-Myc+ Notch1 T-ALL initiating cells

Project description:Missense FBXW7 mutations are prevalent in various tumors, including T-cell acute lymphoblastic leukemia (T-ALL). To study the effects of such lesions, we generated animals carrying regulatable Fbxw7 mutant alleles. We show here that these mutations specifically bolster cancer-initiating cell activity in collaboration with Notch1 oncogenes, but spare normal hematopoietic stem cell function. We were also able to show that FBXW7 mutations specifically affect the ubiquitylation and half-life of c-Myc protein, a key T-ALL oncogene. Using animals carrying c-Myc fusion alleles, we connected Fbxw7 function to c-Myc abundance and correlated c-Myc expression to leukemia-initiating activity. Three independent Notch1 T-ALL were derived on c-Myc-GFP background and sorted from the spleen of leukemic mice on the basis of GFP expression for RNA extraction and hybridization on Affymetrix microarrays

2013-05-10 | E-GEOD-46797 | biostudies-arrayexpress

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Project description:To identify novel down-stream effectors of Notch1 signaling, we have employed cDNA microarray expression profiling as a discovery platform. Human follicualr thyroid carcinoma cell line FTC236 was engineered with tet-on inducible system to establish a stable cell line. The stable cell line FTC236-Notch1 showed robust inducibility with doxycycline, which triggers the expression of Notch1 intracellular domain (NICD). The mRNA samples from FTC236-Notch1 cells with or without doxycline treamtment were analyzed in this assay. Top 50 gene sequences were identified as of the most significance which distinguished between doxycycline treated samples and control samples. Expression of SERPINE1, a down-regulated gene duing Notch1 activation from this signature, was quantified in the same RNA samples by real-time PCR. The protein level was further confirmed by Western blot that restoration of NICD inhibits the expression of SERPINE1.

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The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model

Project description:This SuperSeries is composed of the following subset Series: GSE26789: The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (ALL-B and ALL-T) GSE26790: The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (TOM-1 and MOLT-4) GSE26791: The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (Illumina) GSE26792: The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (SNP) Refer to individual Series

2012-04-17 | E-GEOD-26807 | biostudies-arrayexpress

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