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Homo sapiens

ABSTRACT: Drug-tolerant cancer cell persisters survive lethal exposures by silencing transposable elements [ChIP-Seq]

PROVIDER: PRJNA301677 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2927100_1.fastq.gz	Fastqsanger.gz
	SRR2927100_2.fastq.gz	Fastqsanger.gz
	SRR2927101_1.fastq.gz	Fastqsanger.gz
	SRR2927101_2.fastq.gz	Fastqsanger.gz
	SRR2927102_1.fastq.gz	Fastqsanger.gz

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Repression of stress-induced LINE-1 expression protects cancer cell populations from lethal drug-exposures [ATAC-Seq]

Project description:Establishing and maintaining phenotypic heterogeneity within cell and organismal populations is an evolutionarily conserved strategy that ensures survival of the population following stressful exposures. We previously identified a transient, reversible, drug-tolerant cancer cell subpopulation that survives otherwise lethal drug exposures. Here we show that these drug-tolerant persisters (DTPs) assume a highly heterochromatic state, which requires factors that modify or bind trimethylated H3 lysine 9 (H3K9me3). The increased H3K9me3 in DTPs is largely restricted to evolutionarily young Long Interspersed Repeat elements (LINEs). This transcriptionally repressive state, which decreases the expression of these retrotransposable elements, is critical for DTP survival, and disruption of this heterochromatic state results in re-expression of LINE elements and ablation of this subpopulation. Together, these findings establish a role for epigenetic silencing of transposable elements as a population survival strategy to maintain genomic integrity in subpopulations of cancer cells during lethal drug exposures.

2017-07-03 | GSE73874 | GEO

Drug-tolerant cancer cell persisters survive lethal exposures by silencing transposable elements [ChIP-Seq]

2017-07-03 | GSE74179 | GEO

An isogenic E. coli population gives rise to multiple persister phenotypes

Project description:Antibiotic treatment typically eliminates a significant portion of a bacterial population, leaving behind a smaller subset of tolerant cells that can survive the treatment. These tolerant cells hinder the effectiveness of the antibiotic, potentially leading to the development of antibiotic resistance within the population. Antibiotic tolerance differs from resistance: tolerant cells are unable to grow or reproduce in the presence of the antibiotic, but they can proliferate once the antibiotic is removed. However, in cases of resistance, the antibiotic loses its efficacy entirely, posing a significant threat to public health. Our study challenges the long-held consensus that persisters are completely dormant and are of one single population. Our results clearly show that persisters are not as dormant as once thought, and multiple populations of persisters form during lethal antibiotic treatment despite the cells being genetically identical. We compared the transcriptome profiles at different time points to investigate the dynamic changes and/or existence of multiple persister subpopulations in response to lethal antibiotic ampicillin (Amp) and ciprofloxacin (Cip) treatment in E. coli.

2024-06-21 | GSE256167 | GEO

Mutation independent activation of the Notch pathway is associated with Lapatinib resistance in Her2+ breast cancer cell lines

Project description:We compared untreated HCC1419 cells with Lapatinib resistant HCC1419 cells that were either treated with Lapatinib for only 9 days before harvesting (drug tolerant persisters, DTPs) or were growing in the presence of Lapatinib (>70 days) (drug tolerant expanded persisters, DTEPs). We show that the Notch pathway is significantly over-expressed in DTEPs when compared to untreated cells.

2015-01-15 | GSE62074 | GEO

Mutation independent activation of the Notch pathway is associated with Lapatinib resistance in Her2+ breast cancer cell lines

2015-01-15 | E-GEOD-62074 | biostudies-arrayexpress

Salmonella persisters undermine host immune defences during antibiotic treatment

Project description:Many bacterial infections are hard to treat and tend to relapse, possibly due to the presence of antibiotic-tolerant persisters that are considered dormant cells when bacteria are grown in laboratory medium. Non-growing persisters also form following uptake of Salmonella by macrophages but their nature is little understood. Here we show that Salmonella persisters arising during macrophage infection maintain an active state. Persisters reprogram macrophages by means of effectors secreted by the SPI-2 Type 3 Secretion System (T3SS), thereby dampening pro-inflammatory innate immune responses and inducing anti-inflammatory macrophage polarisation. Reprogramming allows non-growing Salmonella to survive for extended periods in their host. Persisters undermining the host immune defences might confer an advantage to the pathogen during relapse once the antibiotic pressure is relieved.

2018-12-07 | GSE104785 | GEO

Cycling cancer persisters arise from lineages with distinct transcriptional and metabolic programs

Project description:Non-genetic mechanisms have recently emerged as important drivers of therapy failure in cancer, where some cancer cells can enter a reversible drug-tolerant persister state in response to treatment. While most cancer persisters, like their bacterial counterparts, remain arrested in the presence of drug, a rare subset of cancer persisters can re-enter the cell cycle under constitutive drug treatment. Little is known about the non-genetic mechanisms that enable cancer persisters to simultaneously resist therapy and maintain proliferative capacity in the presence of drug. To address this, we developed Watermelon, a new high-complexity expressed barcode lentiviral library for simultaneous tracing each cell's clonal origin, proliferative state, and transcriptional state, and used it to study this rare, transiently-resistant, proliferative persister population and identify what distinguishes it from non-cycling persisters. Analysis of Watermelon-transduced cancer cell lines demonstrated that cycling and non-cycling persisters arise from different pre-existing cell lineages with distinct transcriptional and metabolic programs. The proliferative capacity of persisters is associated with an upregulation of antioxidant gene programs and a metabolic shift to fatty acid oxidation in specific subpopulations of tumor cells.

2020-05-21 | GSE150949 | GEO

The Ontogeny and Vulnerabilities of Lapatinib Drug Tolerant Persisters

Project description:The Ontogeny and Vulnerabilities of Lapatinib Drug Tolerant Persisters

| PRJNA649424 | ENA

Functional screening implicates miR-371-3p and peroxiredoxin 6 in reversible tolerance to cancer drugs [SPR899]

Project description:Acquired resistance to cancer drug therapies almost always occurs in advanced-stage patients even following a significant response to treatment. In addition to mutational mechanisms, various non-mutational resistance mechanisms have now been recognized. We previously described a chromatin-mediated subpopulation of reversibly drug-tolerant persisters (DTPs) that is dynamically maintained within a wide variety of tumor cell populations. Here, we explored a potential role for microRNAs in such transient drug tolerance. Functional screening of 879 human microRNAs revealed miR-371-3p as a potent suppressor of drug tolerance. PRDX6 (peroxiredoxin 6) was identified as a key target of miR-371-3p in establishing drug tolerance by regulating PLA2/PKCÎ± activity and reactive oxygen species. PRDX6 expression is associated with poor prognosis in cancers of multiple tissue origins. These findings implicate miR-371-3p as a suppressor of PRDX6 and suggest that co-targeting of PRDX6 or modulating miR-371-3p expression together with targeted cancer therapies may delay or prevent acquired drug resistance. Drug tolerant persisters (DTPs) generated in response to erlotinib treatment were the basis for RNA extraction and hybridization on Affymetrix microarrays. PC9 cells were treated with DMSO or Erlotinib for 9 days to generate DTPs, then RNA was isolated for analyzing the differential gene expression pattern in DTPs compared to parental cells.

2016-08-01 | E-GEOD-83118 | biostudies-arrayexpress

The Ontogeny and Vulnerabilities of Lapatinib Drug Tolerant Persisters [Parental (P) vs. Drug-Tolerant Persister (DTP)]

Project description:The Ontogeny and Vulnerabilities of Lapatinib Drug Tolerant Persisters [Parental (P) vs. Drug-Tolerant Persister (DTP)]

| PRJNA649434 | ENA