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ULK3 is a key determinant of the keratinocyte self-renewal and tumorigenesis [shULK3 HKCs]

ABSTRACT: ULK3 is a key determinant of the keratinocyte self-renewal and tumorigenesis [shULK3 HKCs]

PROVIDER: PRJNA759140 | ENA |

REPOSITORIES: ENA

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ULK3 is a key determinant of the keratinocyte self-renewal and tumorigenesis

Project description:ULK3 is a key determinant of the keratinocyte self-renewal and tumorigenesis

| PRJNA759135 | ENA

ULK3 is a key determinant of the keratinocyte self-renewal and tumorigenesis [shULK3 SCC13]

Project description:ULK3 is a key determinant of the keratinocyte self-renewal and tumorigenesis [shULK3 SCC13]

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ULK3 is a key determinant of the keratinocyte self-renewal and tumorigenesis

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

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ULK3 is a key determinant of the keratinocyte self-renewal and tumorigenesis [shULK3 SCC13]

Project description:Transcriptomic profiling of human squamous cell carcinoma cells SCC13 infected with three ULK3 silencing lentivirus versus control virus

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ULK3 is a key determinant of the keratinocyte self-renewal and tumorigenesis [shULK3 HKCs]

Project description:Transcriptomic profiling of three strains of primary human keratinocytes infected with two ULK3 silencing lentivirus versus control virus

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The ULK3 kinase is a key determinant of keratinocyte self-renewal and tumorigenesis targeting the arginine methylome

Project description:Epigenetic mechanisms oversee epidermal homeostasis and oncogenesis. The identification of kinases controlling these processes has direct therapeutic implications. We show that ULK3 is a nuclear kinase with elevated expression levels in squamous cell carcinomas (SCCs) arising in multiple body sites, including skin and Head/Neck. ULK3 loss by gene silencing or deletion reduces proliferation and clonogenicity of human keratinocytes and SCC-derived cells and affects transcription impinging on stem cell-related and metabolism programs. Mechanistically, ULK3 directly binds and regulates the activity of two histone arginine methyltransferases, PRMT1 and PRMT5 (PRMT1/5), with ULK3 loss compromising PRMT1/5 chromatin association to specific genes and overall methylation of histone H4, a shared target of these enzymes. These findings are of translational significance, as downmodulating ULK3 by RNA interference or locked antisense nucleic acids (LNAs) blunts the proliferation and tumorigenic potential of SCC cells and promotes differentiation in two orthotopic models of skin cancer.

2022-11-14 | MTBLS5155 | MetaboLights

Erythropoietin promotes breast tumorigenesis through tumor initiating cell self-renewal

Project description:The erythropoietin (EPO) hormone induces red blood cell production and its recombinant form is the most prescribed drug for the treatment of anemia, including that arising in cancer patients. Based on randomized trials showing that EPO administration to cancer patients result in a decreased survival, we investigated the impact of EPO modulation on tumorigenesis. Using genetically engineered mouse models of breast cancer we found that EPO promoted tumorigenesis by activating JAK/STAT signaling specifically in breast tumor initiating cells (TICs) and promoting their self-renewal. Moreover, we define an active role for endogenous EPO in breast cancer progression and breast TIC self-renewal and demonstrate a potential application of EPO pathway inhibition in breast cancer therapy. reference x sample

2014-05-31 | E-GEOD-51433 | biostudies-arrayexpress

The ULK3 kinase is a determinant of keratinocyte self-renewal and tumorigenesis targeting the arginine methylome.

| S-EPMC9935893 | biostudies-literature

Erythropoietin promotes breast tumorigenesis through tumor initiating cell self-renewal

2014-05-31 | GSE51433 | GEO

Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation

Project description:Notch signaling promotes commitment of keratinocytes to differentiation and suppresses tumorigenesis. p63, a p53 family member, has been implicated in establishment of the keratinocyte cell fate and/or maintenance of epithelial self-renewal. Here we show that p63 expression is suppressed by Notch1 activation in both mouse and human keratinocytes through a mechanism independent of cell cycle withdrawal and requiring down-modulation of selected interferon-responsive genes, including IRF7 and/or IRF3. In turn, elevated p63 expression counteracts the ability of Notch1 to restrict growth and promote differentiation. p63 functions as a selective modulator of Notch1-dependent transcription and function, with the Hes-1 gene as one of its direct negative targets. Thus, a complex cross-talk between Notch and p63 is involved in the balance between keratinocyte self-renewal and differentiation. Keywords: Notch1, p63, keratinocyte differentiation, gene expression profiling

2006-07-08 | GSE5229 | GEO

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