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Cell cycle duration determines oncogenic transformation capacity

ABSTRACT: Cell cycle duration determines oncogenic transformation capacity

PROVIDER: PRJNA1026993 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26359915.fastq.gz	Fastqsanger.gz
	SRR26359916.fastq.gz	Fastqsanger.gz

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Cell cycle duration determines oncogenic transformation capacity

Project description:We present single-cell RNA sequencing data of P8 mouse retina with Rb/p107 double knockout (DKO), or Rb/p107 DKO with Skp2+/-.

2025-03-03 | GSE245137 | GEO

A Tunable Mechanism Determines the Transgenerational Duration of Small RNA Inheritance in C.elegans

Project description:In C.elegans nematodes small RNAs enable transmission of epigenetic responses across multiple generations. While RNA interference (RNAi) inheritance mechanisms that enable “memorization” of ancestral responses are being elucidated, it is not known why or how, after a few generations, epigenetic effects are “forgotten”. We show that exposure to dsRNA activates a feedback loop that determines the duration of inherited silencing. We find that gene-specific RNAi responses dictate the transgenerational duration of RNAi responses mounted against unrelated genes, elicited separately in previous generations. RNA-seq analysis reveals that aside from silencing of genes with complementary sequences, dsRNA-induced RNAi affects the production of heritable endogenous small RNAs, which regulate the expression of RNAi factors. Manipulating genes in this feedback pathway changes the duration of heritable silencing. Active control of transgenerational effects could be adaptive, since ancestral responses would be detrimental if the environments of the progeny and the ancestors would differ.

2016-03-24 | GSE77654 | GEO

Epigenetic enhancer changes during oncogenic transformation

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Reprogramming-associated aberrant DNA methylation determines hematopoietic differentiation capacity of human induced pluripotent stem cells

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STRIPAK directs PP2A activity to promote oncogenic transformation

Project description:We evaluated the effects of suppressing MAP4K4 on transcriptome and YAP1 pathway based on the observation that partial suppression of MAP4K4 leads to transformation through activation of YAP1. Mutations and deletions involving subunits of the serine-threonine phosphatase PP2A occur in a broad range of human cancers, and partial loss of PP2A function contributes to cell transformation. In particular, displacement of regulatory B subunits by the viral oncoprotein SV40 small-t antigen (ST) or mutation or deletion of PP2A subunits alters the abundance and types of PP2A complexes in cells and induces cell transformation in human cells. Here we show that ST not only displaces common PP2A B subunits but also promotes PP2A A-C subunit interactions with a set of alternative B subunits (B’’’, striatins) that are components of the Striatin-interacting phosphatase and kinase (STRIPAK) complex. We found that members of the STRIPAK complex are required for ST-PP2A induced cell transformation. PP2A interacts with and dephosphorylates the STRIPAK-associated kinase MAP4K4, which induces cell transformation in part through the regulation of the Hippo pathway effector YAP1. These observations identify an unanticipated role of MAP4K4 in transformation and show that the STRIPAK complex plays a key role in defining PP2A specificity and activity.

2019-12-01 | GSE118272 | GEO

Pulse Duration

Project description:Nimble vs. Torpid Responders: differential adaptations to hydration pulse duration among soil microbes

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Upregulation of Antioxidant Capacity and Nucleotide Precursor Availability Suffices for Oncogenic Transformation.

Project description:The emergence of cancer from diverse normal tissues has long been rationalized to represent a common set of fundamental processes. However, these processes are not fully defined. Here, we show that forced expression of glucose-6-phosphate dehydrogenase (G6PD) affords immortalized mouse and human cells anchorage-independent growth in vitro and tumorigenicity in animals. Mechanistically, G6PD augments the NADPH pool by stimulating NAD+ kinase-mediated NADP+ biosynthesis in addition to converting NADP+ to NADPH, bolstering antioxidant defense. G6PD also increases nucleotide precursor levels through the production of ribose and NADPH, promoting cell proliferation. Supplementation of antioxidants or nucleosides suffices to convert immortalized mouse and human cells into a tumorigenic state, and supplementation of both is required when their overlapping metabolic consequences are minimized. These results suggest that normal cells have a limited capacity for redox balance and nucleotide synthesis, and overcoming this limit might represent a key aspect of oncogenic transformation.

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A methyltransferase-independent role for METTL1 in tRNA aminoacylation and oncogenic transformation

Project description:Data supporting the manuscript: A methyltransferase-independent role for METTL1 in tRNA aminoacylation and oncogenic transformation

2024-11-05 | MSV000096296 | MassIVE

Kim et al. STRIPAK directs PP2A activity towards MAP4K4 to promote oncogenic transformation

Project description:STRIPAK directs PP2A activity towards MAP4K4 to promote oncogenic transformation

2019-10-04 | MSV000084422 | MassIVE

Epigenetic enhancer changes during oncogenic transformation [ChIP-seq]

Project description:Identification of differential enhancers active during oncogenic transformation, using FAIRE-seq and ChIP-seq for H3K4me1 and H3K27ac

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