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BCL-2 levels do not predict azathioprine treatment response in inflammatory bowel disease, but inhibition induces lymphocyte apoptosis and ameliorates colitis in mice.

ABSTRACT: BCL-2 levels do not predict azathioprine treatment response in inflammatory bowel disease, but inhibition induces lymphocyte apoptosis and ameliorates colitis in mice.

PROVIDER: PRJEB26600 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2561380.fastq.gz	Fastqsanger.gz
	ERR2561381.fastq.gz	Fastqsanger.gz
	ERR2561382.fastq.gz	Fastqsanger.gz
	ERR2561383.fastq.gz	Fastqsanger.gz
	ERR2561384.fastq.gz	Fastqsanger.gz

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BCL-2 levels do not predict azathioprine treatment response in inflammatory bowel disease, but inhibition induces lymphocyte apoptosis and ameliorates colitis in mice.

Project description:Background: Inducing apoptosis of autoreactive lymphocytes is part of the therapeutic strategy for Crohn’s disease (CD) patients. Failure to respond to medical therapies upon inflammatory bowel disease could result from insufficient apoptosis. To date there are no useful molecular factors for the prediction of clinical relapse. Study Aims: Characterization of the BCL-2 family-related risk of therapy resistance and verifying its usefulness as parameter for the prediction of clinical relapse could be helpful in deciding which medical therapy to recommend. The project is directly targeted to develop rapidly therapeutic improvement for patients with IBD. A long-term goal is the development of new therapeutic options for the treatment of IBD via a physiologic homeostasis and turnover of lymphocytes. Study Design: We propose to characterize the BCL-2 family-related risk of therapy resistance and its usefulness as parameter for the prediction of clinical relapse upon medical therapy. Samples will be used for next generation sequencing, qPCR, WB, immunohistochemistry and immunofluorescence. The hypothesis is considered confirmed if expression of BCL-2 family members in human peripheral blood is significantly changed between patient groups and correlates with the number of lymphocyte subpopulations.

2018-05-14 | E-MTAB-6739 | biostudies-arrayexpress

Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [WES]

Project description:Glioblastoma multiforme (GBM) is the most aggressive type of brain tumor with poor survival rate and temozolomide (TMZ) has been used as the standard chemotherapy for GBM treatment. However, a large number of patients either respond poorly to TMZ and/or develop resistance after long-term use, urging the need for the development of potent drugs with novel mechanisms of action. Here, using high-throughput compound screening (HTS), we found azathioprine, an immunosuppressive medication, to be a promising therapeutic agent for TMZ-resistant GBM treatment. Through integrative genome-wide analysis and global proteomic analysis, we identified the elevated lipid metabolism due to hyperactive EGFR/AKT/SREBP-1 signaling pathway being inhibited by azathioprine. In addition, azathioprine causes ER stress-induced apoptosis. Orthotopic xenograft models injected with patient-derived GBM cells exhibits reduced tumor volumes and increased apoptosis by azathioprine. These overall data indicate that azathioprine could be a powerful therapeutic option for TMZ-resistant GBM patients.

2021-02-16 | GSE153680 | GEO

Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [microarray]

Project description:Expression profiling of 559T(proneural subtype of glioblastoma), 592T(mesenchymal subtype of glioblastoma) and normal human astrocyte (NHA) Glioblastoma multiforme (GBM) is the most aggressive type of brain tumor with poor survival rate and temozolomide (TMZ) has been used as the standard chemotherapy for GBM treatment. However, a large number of patients either respond poorly to TMZ and/or develop resistance after long-term use, urging the need for the development of potent drugs with novel mechanisms of action. Here, using high-throughput compound screening (HTS), we found azathioprine, an immunosuppressive medication, to be a promising therapeutic agent for TMZ-resistant GBM treatment. Through integrative genome-wide analysis and global proteomic analysis, we identified the elevated lipid metabolism due to hyperactive EGFR/AKT/SREBP-1 signaling pathway being inhibited by azathioprine. In addition, azathioprine causes ER stress-induced apoptosis. Orthotopic xenograft models injected with patient-derived GBM cells exhibits reduced tumor volumes and increased apoptosis by azathioprine. These overall data indicate that azathioprine could be a powerful therapeutic option for TMZ-resistant GBM patients.

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Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [RNA-Seq]

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Transcription profiling of human lymphocyte response to E. coli to identify any transcriptional component to the protection in vitro bacterially induced PBMC apoptosis

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2024-03-12 | PXD049976 | Pride

Phosphorylation of Bcl-xL by ERK1

Project description:The anti-apoptotic function of Bcl-xL in the heart against reperfusion injury is diminished by K-Ras-Mst1-mediated phosphorylation of Ser14, which allows dissociation of Bcl-xL from Bax and promotes cardiomyocyte death. Here we show that Ser14 phosphorylation of Bcl-xL is also promoted by hemodynamic stress in the heart, through the H-Ras-ERK pathway. Our study suggests that phosphorylation of Bcl-xL at Ser14 in response to acute pressure overload plays an essential role in mediating compensatory hypertrophy by promoting calcium release, alleviating the negative constraint of Bcl-xL upon the IP3R-NFAT pathway.

2023-09-06 | PXD045118 | Pride

Development and crystal structures of a more potent second-generation dual degrader of BCL-2 and BCL-xL

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Bcl-2 overexpression effects in rat neural precursor cells.

Project description:Bcl-2 is highly enriched in the nervous system during neural development and plays an important role in modulating cell survival. In addition to its anti-apoptotic function, Bcl-2 has previously been suggested as a mediator of neuronal differentiation. However, the mechanism by which Bcl-2 might influence neurogenesis is not sufficiently understood. We aimed to determine the non-apoptotic functions of Bcl-2 during neuronal differentiation.

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miRNAs expression in HepG2 hepatocellular carcinoma cell lines: Vector Control vs. Twist1, Bcl-2, and Twist1/Bcl-2 Transfected

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