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Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer [scRNA-seq]

ABSTRACT: Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer [scRNA-seq]

PROVIDER: PRJNA979215 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24807372.fastq.gz	Fastqsanger.gz
	SRR24807373.fastq.gz	Fastqsanger.gz
	SRR24807374.fastq.gz	Fastqsanger.gz
	SRR24807375.fastq.gz	Fastqsanger.gz

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Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer

Project description:Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer

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Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer (WGS)

Project description:Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer (WGS)

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Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer [CUT&RUN]

Project description:Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer [CUT&RUN]

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Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer [bulk RNA-seq]

Project description:Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer [bulk RNA-seq]

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Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer

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

2024-03-01 | GSE234033 | GEO

Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer (WGS)

Project description:Telomere dysfunction drives chromosomal instability (CIN) during the transition from benign adenoma to malignant adenocarcinoma. While CIN provides a mutator mechanism for cancer- relevant genomic events, its role in shaping tumor biology during carcinogenesis is not well understood. Here, we explored the molecular and biological impact of telomere dysfunction and associated CIN in vivo in a faithful model of CRC. In vivo lineage tracing revealed that CIN increased the rate of neoplastic cell clonal expansion through accelerated differentiation of neighboring stem cells, resulting in increased number of adenomas and decreased survival in CIN-high Apcmin mice. Mechanistically, CIN represses EZH2 leading to upregulation of secreted Wnt antagonists, which resulted in a growth advantage to CIN-high neoplastic cells. Correspondingly, pharmacological activation of intrinsic WNT signaling enhanced intestinal stem cells fitness, leading to reduced neoplastic cell clonal expansion and adenoma burden. Thus, the CIN-EZH2-WNT axis enhances intestinal cancer initiation in the nascent tumor microenvironment, providing a preventive strategy for patients harboring germline APC mutations.

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Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer [scRNA-seq]

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Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer [CUT&RUN]

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Telomeric Chromosomal Instability Fosters Paracrine Mediated Cell Competition to Initiate Intestinal Cancer [bulk RNA-seq]

2024-03-01 | GSE234032 | GEO

Mammalian telomeres reforged with non-telomeric sequences

Project description:Telomere is a highly refined system for maintaining the stability of linear chromosomes. Most telomeres rely on simple repetitive sequences and telomerase enzymes, but in some species or telomerase-defective situations, alternative telomere lengthening (ALT) mechanism is utilized to protect chromosomal ends. Telomere loss can induce telomere recombination by which specific sequences can be recruited into telomeres. However, canonical telomeric repeat-based telomeres have been found in mammals. Here, we show that mammalian telomeres can also be completely reconstituted using a non-telomeric unique sequence. We found that a specific subtelomeric element, named as mouse template for ALT (mTALT), is utilized for repairing telomeric DNA damage and composing new telomeric sequences in mouse embryonic stem cells. We found a high-level of non-coding mTALT transcript despite the heterochromatic nature of mTALT-based telomere. After ALT activation, the increased HMGN1, a non-histone chromosomal protein, contributed to maintaining telomere stability by regulating telomeric transcriptions. Our findings reveal novel molecular features of potential telomeric sequences which can reconstitute telomeres during cancer formation and evolution.

2020-07-17 | MSV000085772 | MassIVE

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