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Revealing role of epigenetic modifers and DNA oxidation in cell‐autonomous regulation of Cancer stem cells

ABSTRACT: Revealing role of epigenetic modifers and DNA oxidation in cell‐autonomous regulation of Cancer stem cells

PROVIDER: PRJNA1084012 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28230840_1.fastq.gz	Fastqsanger.gz
	SRR28230840_2.fastq.gz	Fastqsanger.gz
	SRR28230841_1.fastq.gz	Fastqsanger.gz
	SRR28230841_2.fastq.gz	Fastqsanger.gz
	SRR28230842_1.fastq.gz	Fastqsanger.gz

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Revealing role of epigenetic modifers and DNA oxidation in cell‐autonomous regulation of Cancer stem cells

Project description:Breast cancer cells (BCCs) can remain undetected for decades in dormancy. These quiescent cells are similar to cancer stem cells (CSCs); hence their ability to initiate tertiary metastasis. Dormancy can be regulated by components of the tissue microenvironment such as bone marrow mesenchymal stem cells (MSCs) that release exosomes to dediferentiate BCCs into CSCs. The exosomes cargo includes histone 3, lysine 4 (H3K4) methyltransferases - KMT2B and KMT2D. A less studied mechanism of CSC maintenance is the process of cell-autonomous regulation, leading us to examine the roles for KMT2B and KMT2D in sustaining CSCs, and their potential as drug targets.

2025-01-02 | GSE260924 | GEO

Revealing role of epigenetic modifiers and DNA oxidation in cell-autonomous regulation of Cancer stem cells.

Project description:BackgroundBreast cancer cells (BCCs) can remain undetected for decades in dormancy. These quiescent cells are similar to cancer stem cells (CSCs); hence their ability to initiate tertiary metastasis. Dormancy can be regulated by components of the tissue microenvironment such as bone marrow mesenchymal stem cells (MSCs) that release exosomes to dedifferentiate BCCs into CSCs. The exosomes cargo includes histone 3, lysine 4 (H3K4) methyltransferases - KMT2B and KMT2D. A less studied mechanism of CSC maintenance is the process of cell-autonomous regulation, leading us to examine the roles for KMT2B and KMT2D in sustaining CSCs, and their potential as drug targets.MethodsUse of pharmacological inhibitor of H3K4 (WDR5-0103), knockdown (KD) of KMT2B or KMT2D in BCCs, real time PCR, western blot, response to chemotherapy, RNA-seq, and flow cytometry for circulating markers of CSCs and DNA hydroxylases in BC patients. In vivo studies using a dormancy model studied the effects of KMT2B/D to chemotherapy.ResultsH3K4 methyltransferases sustain cell autonomous regulation of CSCs, impart chemoresistance, maintain cycling quiescence, and reduce migration and proliferation of BCCs. In vivo studies validated KMT2's role in dormancy and identified these genes as potential drug targets. DNA methylase (DNMT), predicted within a network with KMT2 to regulate CSCs, was determined to sustain circulating CSC-like in the blood of patients.ConclusionH3K4 methyltransferases and DNA methylation mediate cell autonomous regulation to sustain CSC. The findings provide crucial insights into epigenetic regulatory mechanisms underlying BC dormancy with KMT2B and KMT2D as potential therapeutic targets, along with standard care. Stem cell and epigenetic markers in circulating BCCs could monitor treatment response and this could be significant for long BC remission to partly address health disparity.

| S-EPMC10863086 | biostudies-literature

Carnitine Palmitoyltransferase 1 facilitates fatty acid oxidation in a noncell autonomous manner [TKO_RNAseq]

Project description:Carnitine Palmitoyltransferase 1 facilitates fatty acid oxidation in a noncell autonomous manner [TKO_RNAseq]

| PRJNA1113638 | ENA

Carnitine Palmitoyltransferase 1 facilitates fatty acid oxidation in a noncell autonomous manner [CPT1a_RNAseq]

Project description:Carnitine Palmitoyltransferase 1 facilitates fatty acid oxidation in a noncell autonomous manner [CPT1a_RNAseq]

| PRJNA1113636 | ENA

Acetate oxidation

Project description:Acetate oxidation

| PRJNA1033353 | ENA

Cell non-autonomous regulation of chromosome segregation

Project description:Cell non-autonomous regulation of chromosome segregation

| PRJNA435867 | ENA

Carnitine Palmitoyltransferase 1 facilitates fatty acid oxidation in a noncell autonomous manner [CPT1a_RNAseq]

Project description:Mitochondrial fatty acid oxidation is facilitated by the combined activities of Carnitine Palmitoyltransferase 1 and Carnitine Palmitoyltransferase 2 which generate and utilize acylcarnitines respectively. We compared the response of mice with liver specific deficiencies in the liver enriched Cpt1a or the ubiquitous Cpt2 and discovered that they display unique metabolic, physiological and molecular phenotypes. The loss of Cpt1a or Cpt2 resulted in the induction of the muscle enriched isoenzyme, Cpt1b, in hepatocytes in a Ppara dependent manner. Primary component analysis also revealed overall differential grouping between mouse with deletions of either Cpt1a or Cpt2. Our results utilize stringent genetic mouse models to elucidate that the sequential steps to facilitate mitochondrial fatty acid oxidation may have other factors.

2024-05-31 | GSE267915 | GEO

Autonomous and non-autonomous functions of IL10RA in intestinal macrophages

Project description:Autonomous and non-autonomous functions of IL10RA in intestinal macrophages

| PRJNA872263 | ENA

Cell non-autonomous regulation of chromosome segregation

Project description:Chromosome segregation has been assumed to be a cell-autonomous process. We tested this assumption by comparing chromosome segregation fidelity in epithelial cells in various contexts and discovered that these cells have increased chromosome missegregation outside of their native tissue. Using organoid culture systems, we show that tissue architecture, specifically integrin function, is required for accurate chromosome segregation in epithelia. We find that tissue architecture enhances the correction of merotelic microtubule-kinetochore attachments, and this is critically important for maintaining chromosome stability in the polyploid liver. Our data lead to the surprising conclusion that chromosome segregation in epithelia is a cell non-autonomous process. We propose that disruption of tissue architecture could underlie the chromosome instability that characterizes and drives epithelial cancers. Moreover, our findings highlight the importance of context for fundamental cellular processes and caution against the exclusive reliance on cell culture systems for deciphering and manipulating mammalian biology.

2018-08-23 | GSE111078 | GEO

On the epigenetic role of guanosine oxidation.

Project description:Chemical modifications of DNA and RNA regulate genome functions or trigger mutagenesis resulting in aging or cancer. Oxidations of macromolecules, including DNA, are common reactions in biological systems and often part of regulatory circuits rather than accidental events. DNA alterations are particularly relevant since the unique role of nuclear and mitochondrial genome is coding enduring and inheritable information. Therefore, an alteration in DNA may represent a relevant problem given its transmission to daughter cells. At the same time, the regulation of gene expression allows cells to continuously adapt to the environmental changes that occur throughout the life of the organism to ultimately maintain cellular homeostasis. Here we review the multiple ways that lead to DNA oxidation and the regulation of mechanisms activated by cells to repair this damage. Moreover, we present the recent evidence suggesting that DNA damage caused by physiological metabolism acts as epigenetic signal for regulation of gene expression. In particular, the predisposition of guanine to oxidation might reflect an adaptation to improve the genome plasticity to redox changes.

| S-EPMC6926346 | biostudies-literature

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