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Effect of MS-275 and CXD101 on gene expression of M-MDSCs and PMN-MDSCs [RNA-Seq]

ABSTRACT: Effect of MS-275 and CXD101 on gene expression of M-MDSCs and PMN-MDSCs [RNA-Seq]

PROVIDER: PRJNA971509 | ENA |

REPOSITORIES: ENA

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Effect of MS-275 and CXD101 on gene expression of M-MDSCs and PMN-MDSCs [RNA-Seq]

Project description:To elucidate the molecular mechanisms of HDAC1-3 inhibitors in inhibiting M-MDSCs, RNA-seq analysis of M-MDSCs and PMN-MDSCs isolated from Hepa 1-6 tumor-bearing mice treated with MS-275 or CXD101 were performed.

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Effect of MS-275 and CXD101 on open chromatin regions of M-MDSCs [ATAC-seq]

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MS-275 and Isotretinoin in Treating Patients With Metastatic or Advanced Solid Tumors or Lymphomas

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MS-275 in Treating Patients With Advanced Solid Tumors or Lymphoma

Project description:RATIONALE: MS-275 may stop the growth of cancer cells by blocking the enzymes necessary for their growth. PURPOSE: This phase I trial is studying the side effects and best dose of MS-275 in treating patients with advanced solid tumors or lymphoma.

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Transcriptome comparison of PMN-MDSCs and and normal neutrophils

Project description:Polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC), also named pathologically activated neutrophil, is a critical component of tumor microenvironment (TME), playing crucial roles in tumor progression and therapy resistance. Here, we compared the transcriptome of PMN-MDSCs from B16 tumor bearing mice and the neutrophils from tumor free mice.

2023-06-26 | GSE199601 | GEO

Transcriptome analysis of mouse embryonic stem cells treated with MS-275

Project description:This study describes transcriptome profiling of mouse ES cells treated with MS-275. We included RNA-Seq of ds_cDNA synthesized from double poly(A) selected mRNA RNA-Seq profiling on mouse ES cells treated with MS-275

2014-03-28 | E-GEOD-45909 | biostudies-arrayexpress

Inhibition of histone deacetylation by MS-275 alleviates colitis by activating the vitamin D receptor

Project description:BACKGROUND: Ulcerative colitis (UC) is a common chronic inflammatory bowel disease without curative treatment. METHODS: We conducted gene set enrichment analysis to explore potential therapeutic agent for UC. Human colon tissue samples were collected to test H3 acetylation in UC. Both in vivo and in vitro colitis models were constructed to verify the role and mechanism of H3 acetylation modification in UC. Intestine-specific vitamin D receptor (VDR)-/- mice and VD (vitamin D)-deficient diet-fed mice were used to explore downstream molecular mechanism accordingly. RESULTS: According to the Connectivity Map database, MS-275 (class I histone deacetylase inhibitor) was the top-ranked agent, indicating potential importance of histone acetylation in the pathogenesis of UC. We then found that histone H3 acetylation was significantly decreased in the colon epithelium of UC patients and negatively associated with disease severity. MS-275 treatment inhibited histone H3 deacetylation, and subsequently attenuated nuclear factor kappa B (NF-?B)-induced inflammation, reduced cellular apoptosis, maintained epithelial barrier function, and thereby reduced colitis activity in a mouse model of colitis. We also identified VDR to be a downstream effector of MS-275. The curative effect of MS-275 on colitis was abolished in VDR-/- mice and in VD-deficient diet-fed mice and VDR directly targeted p65. In UC patients, histone H3 acetylation, VDR and zonulin-1 expression showed similar downregulation patterns and were negatively associated with disease severity. CONCLUSION: We demonstrate that MS-275 inhibits histone deacetylation and alleviates colitis by ameliorating inflammation, reducing apoptosis and maintaining intestinal epithelial barrier via VDR, providing new strategies for UC treatment.

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Transcriptome analysis of mouse embryonic stem cells treated with MS-275

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2014-03-28 | GSE45909 | GEO

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