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The novel RNA polymerase I transcription inhibitor PMR-116 exploits a critical therapeutic vulnerability in a broad-spectrum of high MYC malignancies

ABSTRACT: The novel RNA polymerase I transcription inhibitor PMR-116 exploits a critical therapeutic vulnerability in a broad-spectrum of high MYC malignancies

PROVIDER: PRJNA1288473 | ENA |

REPOSITORIES: ENA

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The novel RNA polymerase I transcription inhibitor PMR-116 exploits a critical therapeutic vulnerability in a broad-spectrum of high MYC malignancies

Project description:Ribosome biogenesis (RiBi) is a key determinant of cell growth and proliferation and is highly elevated in cancer due to the activation by oncogenes such as MYC. First-generation RiBi inhibitor CX-5461, while demonstrating clinical potential for cancer treatment, also induces DNA damage through off-target inhibition of TOP2⍺ and potentially other mechanisms, bringing into question RiBi as a target for cancer therapy. In this study, we test second-generation RiBi inhibitor, PMR-116. PMR-116 exhibits improved drug-like properties compared to first-generation RiBi inhibitors and has robust anti-tumour activity in the absence of global DNA damage signalling in a broad range of pre-clinical models of haematologic and solid cancers, particularly in malignancies where MYC is either the driver of disease or is elevated. Thus, our work demonstrates that RiBi is a genuine target for cancer therapy and highlights the potential to exploit a critical therapeutic vulnerability in high-MYC human cancers with dismal therapeutic outcomes.

2025-07-08 | GSE302078 | GEO

The novel RNA polymerase I transcription inhibitor PMR-116 exploits a critical therapeutic vulnerability in a broad-spectrum of high MYC malignancies [ChIP-Seq]

2025-07-08 | GSE302076 | GEO

The novel RNA polymerase I transcription inhibitor PMR-116 exploits a critical therapeutic vulnerability in a broad-spectrum of high MYC malignancies [ChIP-Seq]

Project description:The novel RNA polymerase I transcription inhibitor PMR-116 exploits a critical therapeutic vulnerability in a broad-spectrum of high MYC malignancies [ChIP-Seq]

| PRJNA1288469 | ENA

Pmr, a histone-like protein H1 (H-NS) family protein encoded by the IncP-7 plasmid pCAR1, is a key global regulator that alters host function

Project description:H-NS family proteins are known as a member of nucleoid associated proteins (NAPs) conserved in genus Pseudomonas bacteria. Incompatibility group (Inc) P-7 archetype plasmid pCAR1 is transmissible among various Pseudomonas strains and carries genes encoding H-NS family protein, Pmr. P. putida KT2440 is one of pCAR1 hosts, which possesses five genes encoding H-NS family proteins, PP_1366 (TurA), PP_3765 (TurB), PP_0017 (TurC), PP_3693 (TurD), and PP_2947 (TurE) on its chromosome. Quantitative RT-PCR showed that the presence of Pmr did not affect on the transcriptions of genes encoding H-NS family proteins, and only Pmr, TurA and TurB were majorly transcribed. In vitro Pull down assay revealed that Pmr strongly interacted with Pmr itself and TurA, TurB, and TurE. Transcriptome comparisons of pmr disruptant, with KT2440 and KT2440(pCAR1) showed that the pmr disruption had larger effects on the host transcriptome than those by pCAR1 carriage. The transcriptional levels of some genes increased by pCAR1 carriage were reverted to those of pCAR1-free KT2440 by disruption of pmr, such as mexEFoprN genes for efflux pump, and parI. Transcriptional levels of many genes on the putative foreign DNA regions were not altered by carriage of pCAR1 but by pmr disruption. Identification of genome-wide Pmr binding sites by ChAP-chip analysis showed that Pmr preferentially binds to the foreign DNA region. Pmr binding sites were well overlapping with the location of the differentially transcribed genes by disruption of pmr. Our findings indicate that Pmr is a key factor to optimize the gene transcription onpCAR1 and host chromosome.

2010-05-25 | GSE21968 | GEO

Acinetobacter baumannii strain:PMR-Low

Project description:Acinetobacter baumannii strain:PMR-Low Genome sequencing

| PRJNA530197 | ENA

Acinetobacter baumannii strain:PMR-High

Project description:Acinetobacter baumannii strain:PMR-High Genome sequencing

| PRJNA530202 | ENA

Expression data from dark-grown BR double mutant bzr1-1D;bri1-116, single mutant bri1-116, and wildtype

2010-12-31 | GSE25134 | GEO

Expression data from dark-grown BR double mutant bzr1-1D;bri1-116, single mutant bri1-116, and wildtype

Project description:Molecular genetic analyses support a central role of BZR1 in Brassinosteroid (BR) regulation of plant development. The dominant bzr1-1D mutation, which stabilizes the BZR1 protein, completely suppresses the de-etiolated phenotype of the null bri1-116 mutant grown in the dark. Using microarray analysis, we identified genes differentially expressed in bri1-116 compared to wild type and genes differentially expressed in the bzr1-1D;bri1-116 double mutant compared to the bri1-116 single mutant. Consistent with the phenotypic suppression of bri1-116 by bzr1-1D, about 80% of the genes affected in bri1-116 were affected oppositely by bzr1-1D BZR1 regulated genes were generated from comparing genes differentially expressed by bzr1-1D;bri1-116 and bri1-116. Genes affected by BRI1 were generated from comparing differentially expressed genes of bri1-116 and Col control. ANOVA was used to find genes whose expression was different between bzr1-1D;bri1-116 and bri1-116 or between bri1-116 and Col samples [see Supplementary file below].

2010-12-31 | E-GEOD-25134 | biostudies-arrayexpress

Foxp3 exploits a preexistent enhancer landscape for regulatory T cell lineage specification

Project description:This SuperSeries is composed of the following subset Series: GSE40684: Foxp3 exploits a preexistent enhancer landscape for regulatory T cell lineage specification [ChIP-Seq] GSE40685: Foxp3 exploits a preexistent enhancer landscape for regulatory T cell lineage specification [Expression] Refer to individual Series

2012-09-28 | E-GEOD-40686 | biostudies-arrayexpress

MicroRNA profiling of HCT-116 versus HCT-116 treated with 5-aza-2'-deoxycytidine processing human colon cancer cell lines

Project description:UCRs expression signature of HCT-116 cell lines versus HCT-116 cell line treated with DNA methylation inhibitor 5-aza-2'-deoxycytidine

2010-03-09 | E-MTAB-196 | biostudies-arrayexpress

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