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Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [ATAC-seq]

ABSTRACT: To identify accessible chromatin regions regulated BAF53A in squamous cell carcinomas (SCCs), we performed ATAC-seq in FaDu SCC cell lines after BAF53A knockdown by siRNA and in normal keratinocytes with BAF53A overexpression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE156786 | GEO | 2021/10/29

REPOSITORIES: GEO

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Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [RNA-seq]

Project description:To identify genes regulated by BAF53A, we carried out RNA-seq analysis in three SCC cell lines after BAF53A knockdown by siRNA and in normal keratinocytes with BAF53A overexpression.

2021-10-29 | GSE156785 | GEO

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [CnR]

Project description:To determine whether the chromatin accessibility for YAP/TEADs in squamous cell carcinoma cells is directly regulated by BAF53A within BAF complexes, we performed CUT&RUN to profile the distribution of YAP, TEAD1, and BAF155 (a DNA binding subunit of BAF complexes) across the genome.

2021-10-29 | GSE156787 | GEO

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [CnR]

Project description:Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [CnR]

| PRJNA659023 | ENA

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [ATAC-seq]

Project description:Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [ATAC-seq]

| PRJNA659022 | ENA

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [RNA-seq]

Project description:Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [RNA-seq]

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Expression analyses of inducible c-Fos expressing kerationcytes

Project description:Expression analyses comparing c-Fos expressing keratinocytes vs non-expressing controls. Skin squamous cell carcinomas (SCCs) are the second most prevalent skin cancers. Chronic skin inflammation has been associated with the development of SCCs, but the contribution of skin inflammation to SCC development remains largely unknown. In this study we demonstrate that inducible expression of c-fos in the epidermis of adult mice is sufficient to promote inflammation-mediated epidermal hyperplasia leading to the development of pre-neoplastic lesions. Interestingly, c-Fos transcriptionally controls mmp10 and s100a7a15 expression in keratinocytes subsequently leading to CD4 T cell recruitment to the skin, thereby promoting epidermal hyperplasia. Combining inducible c-fos expression in the epidermis with a single dose of the carcinogen 7,12-Dimethylbenz(a)anthracene (DMBA) leads to the development of highly invasive SCCs, which are prevented by using the anti-inflammatory drug Sulindac. Moreover, human SCCs display a correlation between c-FOS expression and elevated levels of MMP10 and S100A15 proteins as well as CD4 T cell infiltration. Our studies demonstrate a bidirectional crosstalk between pre-malignant keratinocytes and infiltrating CD4 T cells in SCC development. Therefore, targeting inflammation along with the newly identified targets, such as MMP10 and S100A15, represent promising therapeutic strategies to treat SCCs. 5 different time points measured in triplicate comparing Dox-treated vs untreated c-FostetON keratinocytes

2013-09-05 | E-GEOD-50621 | biostudies-arrayexpress

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

Expression analyses of inducible c-Fos expressing kerationcytes

2013-09-05 | GSE50621 | GEO

Expression data from Knockdown of BAF53A in DLD1 cell line

Project description:BAF53A, an important subunit of the SWI/SNF epigenetic chromatin regulatory complex, has been implicated as the driver of diverse cancers. However, the role of BAF53A in colorectal cancer (CRC) remains poorly understood.

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Baf53a is involved in survival of mouse ES cells, which can be compensated by Baf53b.

Project description:The human Baf (Brg1/Brm associated factor) complex, also known as the mammalian SWI/SNF chromatin-remodeling complex, is involved in a variety of cellular processes. The pluripotency and self-renewal abilities are major characteristics of embryonic stem (ES) cells and are regulated by the ES cell-specific BAF (esBAF) complex. Baf53a is one of the subunits of the esBAF complex. Here, we found that growth of Baf53a-deficient ES cells was repressed, and expression of p53, p21, and cleaved Caspase 3 was increased. Interestingly, Baf53b, a homologue of Baf53a, rescued cell death of Baf53a-deficient ES cells. Baf53a-deficient ES cells overexpressing exogenous Baf53a or Baf53b remained in the undifferentiated state and proliferated. In summary, our findings suggest that Baf53a is involved in the survival of ES cells, and that Baf53b is able to compensate for this functional aspect of Baf53a.

2017-11-16 | GSE103694 | GEO

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