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MST-312: a telomerase inhibitor effectively blocking MYC oncogenic functions

ABSTRACT: MST-312: a telomerase inhibitor effectively blocking MYC oncogenic functions

PROVIDER: PRJNA309377 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3110942.fastq.gz	Fastqsanger.gz
	SRR3110943.fastq.gz	Fastqsanger.gz
	SRR3110944.fastq.gz	Fastqsanger.gz

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Similar Datasets

MST-312: a telomerase inhibitor effectively blocking MYC oncogenic functions [array]

Project description:Reactivation of the telomerase reverse transcriptase subunit, TERT, is linked to tumourigenesis due to well-documented telomere-dependent and independent functions. The aim of this study was to investigate the effect of the telomerase inhibitor, MST-312, on TERT functions, focusing in particular, on its effects on MYC stabilty and MYC-regulated pathways, in order to assess its potential as a therapeutic agent. We demonstrate that MST-312 reduces MYC levels in cancer cells, leading to reduced MYC levels on chromatin, and subsequently affecting the MYC-regulated transcriptional program. As a result, MST-312 treatment increases the survival of lymphoma-bearing mice. Mechanistically, MST-312 affects the conformation of TERT, leading to TERT/Terc dissociation, and the subsequent loss of both its telomere-dependent and independent functions. Based on the presented data, we conclude that MST-312 treatment is a promising therapeutic strategy, in particular, in MYC-driven tumorus.

2020-01-01 | GSE77014 | GEO

MST-312: a telomerase inhibitor effectively blocking MYC oncogenic functions [ChIP-Seq]

2020-01-01 | GSE77061 | GEO

MST-312: a telomerase inhibitor effectively blocking MYC oncogenic functions

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

2020-01-01 | GSE77063 | GEO

Genome-wide TNFM-NM-1-induced p65 binding before and after telomerase inhibition in HeLa cells

Project description:Chromatin immunoprecipitation sequencing (ChIP-seq) was performed to analyze the effect of telomerase inhibition on TNFM-NM-1-induced genome-wide p65 binding in HeLa cells. By obtaining over 40 million uniquely mappable reads per sample from ChIP-seq, maps for TNFM-NM-1-induced p65 binding in absence and presence of an hTERT inhibitor, MST-312, were generated. As expected, TNFM-NM-1 treatment significantly increased genome-wide p65 occupancy. Interestingly, when cells were treated with MST-312 prior to TNFM-NM-1 stimulation, the number of p65 binding sites was reduced. In addition, some binding sites, including important p65 targets like IL6 and TNF, showed a reduced p65 occupancy with a minimum fold change of 1.5, after MST-312 exposure. Taken together, our ChIP-seq data indicate that telomerase is required for optimal p65 binding at a small proportion of p65 target sites upon inflammatory stimuli. Examination of p65 binding in HeLa cells in absence and presence of TNFM-NM-1 and MST-312.

2012-11-26 | E-GEOD-41100 | biostudies-arrayexpress

Homo sapiens

Project description:MST-312: a telomerase inhibitor effectively blocking MYC oncogenic functions [array]

| PRJNA309283 | ENA

Genome-wide TNFα-induced p65 binding before and after telomerase inhibition in HeLa cells

Project description:Chromatin immunoprecipitation sequencing (ChIP-seq) was performed to analyze the effect of telomerase inhibition on TNFα-induced genome-wide p65 binding in HeLa cells. By obtaining over 40 million uniquely mappable reads per sample from ChIP-seq, maps for TNFα-induced p65 binding in absence and presence of an hTERT inhibitor, MST-312, were generated. As expected, TNFα treatment significantly increased genome-wide p65 occupancy. Interestingly, when cells were treated with MST-312 prior to TNFα stimulation, the number of p65 binding sites was reduced. In addition, some binding sites, including important p65 targets like IL6 and TNF, showed a reduced p65 occupancy with a minimum fold change of 1.5, after MST-312 exposure. Taken together, our ChIP-seq data indicate that telomerase is required for optimal p65 binding at a small proportion of p65 target sites upon inflammatory stimuli.

2012-11-26 | GSE41100 | GEO

Homo sapiens

Project description:MST-312: a telomerase inhibitor effectively blocking MYC oncogenic functions [ChIP-Seq]

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Gene expression changes by telomere shortening in human colonic organoids

Project description:Gene expression changes of UC-model organoids derive from human colon indcued by telomere enlongation was assessed by Madecassoside treatemt (telomerase activator). Gene expression changes of human colon organoids induced by telomere shortening was assessd by MST-312 treatment (telomerase inhibitor).

2021-06-24 | GSE175994 | GEO

A Bioinformatics Analysis Identifies the Telomerase Inhibitor MST-312 for Treating High-STMN1-Expressing Hepatocellular Carcinoma.

Project description:Hepatocellular carcinoma (HCC) is a relatively chemo-resistant tumor. Several multi-kinase inhibitors have been approved for treating advanced HCC. However, most HCC patients are highly refractory to these drugs. Therefore, the development of more effective therapies for advanced HCC patients is urgently needed. Stathmin 1 (STMN1) is an oncoprotein that destabilizes microtubules and promotes cancer cell migration and invasion. In this study, cancer genomics data mining identified STMN1 as a prognosis biomarker and a therapeutic target for HCC. Co-expressed gene analysis indicated that STMN1 expression was positively associated with cell-cycle-related gene expression. Chemical sensitivity profiling of HCC cell lines suggested that High-STMN1-expressing HCC cells were the most sensitive to MST-312 (a telomerase inhibitor). Drug-gene connectivity mapping supported that MST-312 reversed the STMN1-co-expressed gene signature (especially BUB1B, MCM2/5/6, and TTK genes). In vitro experiments validated that MST-312 inhibited HCC cell viability and related protein expression (STMN1, BUB1B, and MCM5). In addition, overexpression of STMN1 enhanced the anticancer activity of MST-312 in HCC cells. Therefore, MST-312 can be used for treating STMN1-high expression HCC.

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Bacteroidetes MST

Project description:Bacteroidetes pyrosequencing for microbial source tracking (MST)

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