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Dysregulation of MITF in the context of defective MC1R and RB1/p16/CDK4 leads to melanocyte transformation [ChIP-Seq]

ABSTRACT: Chip-seq analysis of immortalized melanocytes Hermes 3c and Hermes 4c derivative cell lines following lentiviral transduction of a HA-tagged MITF-M construct (pLX3xHAvar4mCherry)

ORGANISM(S): Homo sapiens

PROVIDER: GSE142014 | GEO | 2020/07/02

REPOSITORIES: GEO

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Dysregulation of MITF in the context of defective MC1R and RB1/p16/CDK4 leads to melanocyte transformation [RNA-Seq]

Project description:RNAseq Expression analysis of immortalized melanocytes Hermes 3c (3C) and Hermes 4c (4C) cell lines following siRNA transfection with a control scrambled siRNA or an RNA targeting MITF

2020-07-02 | GSE142017 | GEO

Dysregulation of MITF in the context of defective MC1R and RB1/p16/CDK4 leads to melanocyte transformation [microarray]

Project description:Expression analysis of immortalized melanocytes Hermes 3c and Hermes 4c derivative cell lines following lentiviral transduction of a HA-tagged MITF-M construct (pLX3xHAvar4mCherry) or control construct (pLVX IRES mCherry).

2020-07-02 | GSE142012 | GEO

Dysregulation of MITF in the context of defective MC1R and RB1/p16/CDK4 leads to melanocyte transformation

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

2020-07-02 | GSE142018 | GEO

Dysregulation of MITF in the context of defective MC1R and RB1/p16/CDK4 leads to melanocyte transformation

Project description:Dysregulation of MITF in the context of defective MC1R and RB1/p16/CDK4 leads to melanocyte transformation

| PRJNA595574 | ENA

Dysregulation of MITF in the context of defective MC1R and RB1/p16/CDK4 leads to melanocyte transformation [microarray]

Project description:Dysregulation of MITF in the context of defective MC1R and RB1/p16/CDK4 leads to melanocyte transformation [microarray]

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Dysregulation of MITF in the context of defective MC1R and RB1/p16/CDK4 leads to melanocyte transformation [RNA-Seq]

Project description:Dysregulation of MITF in the context of defective MC1R and RB1/p16/CDK4 leads to melanocyte transformation [RNA-Seq]

| PRJNA595577 | ENA

Dysregulation of MITF in the context of defective MC1R and RB1/p16/CDK4 leads to melanocyte transformation [ChIP-Seq]

Project description:Dysregulation of MITF in the context of defective MC1R and RB1/p16/CDK4 leads to melanocyte transformation [ChIP-Seq]

| PRJNA595578 | ENA

Dysregulation of MITF Leads to Transformation in MC1R-Defective Melanocytes.

Project description:The MC1R/cAMP/MITF pathway is a key determinant for growth, differentiation, and survival of melanocytes and melanoma. MITF-M is the melanocyte-specific isoform of Microphthalmia-associated Transcription Factor (MITF) in human melanoma. Here we use two melanocyte cell lines to show that forced expression of hemagglutinin (HA) -tagged MITF-M through lentiviral transduction represents an oncogenic insult leading to consistent cell transformation of the immortalized melanocyte cell line Hermes 4C, being a melanocortin-1 receptor (MC1R) compound heterozygote, while not causing transformation of the MC1R wild type cell line Hermes 3C. The transformed HA-tagged MITF-M transduced Hermes 4C cells form colonies in soft agar and tumors in mice. Further, Hermes 4C cells display increased MITF chromatin binding, and transcriptional reprogramming consistent with an invasive melanoma phenotype. Mechanistically, forced expression of MITF-M drives the upregulation of the AXL tyrosine receptor kinase (AXL), with concomitant downregulation of phosphatase and tensin homolog (PTEN), leading to increased activation of the PI3K/AKT pathway. Treatment with AXL inhibitors reduces growth of the transformed cells by reverting AKT activation. In conclusion, we present a model system of melanoma development, driven by MITF-M in the context of MC1R loss of function, and independent of UV exposure. This model provides a basis for further studies of critical changes in the melanocyte transformation process.

| S-EPMC7408466 | biostudies-literature

The chromatin dynamics of the TFAP2A/ MITF genetic interaction in melanocyte development.

Project description:We have deleted TFAP2A and its redundantly-acting paralog TFAP2C in human melanoma SkMel28 cell lines and are assessing MITF binding using Cleavage Under Targets and Release Using Nuclease (CUT&RUN). Conversely, we deleted all copies of MITF in SkMEL28 cells and are similarly profiling TFAP2A bound loci. We predict TFAP2A functions as a pioneer factor for MITF during melanocyte development and that in the absence of TFAP2A, MITF binding at loci normally co-bound by MITF/TFAP2A will be disrupted.

2023-02-08 | GSE166359 | GEO

The chromatin dynamics of the TFAP2A/ MITF genetic interation in melanocyte development.

Project description:In developing melanocytes and in melanoma cells, multiple paralogs of the Activating-enhancer-binding Protein 2 family of transcription factors (TFAP2) contribute to expression of genes encoding pigmentation regulators, but their interaction with Microphthalmia transcription factor (MITF), a master regulator of these cells, is unclear. Supporting the model that Tfap2 facilitates MITF's ability to activate expression of pigmentation genes, single-cell seq analysis of zebrafish embryos revealed that pigmentation genes are only expressed in the subset of mitfa-expressing cells that also express Tfap2 paralogs. To test this model in SK-MEL-28 melanoma cells we deleted the two TFAP2 paralogs with highest expression, TFAP2A and TFAP2C, creating TFAP2 knockout (TFAP2-KO) cells. We then assessed gene expression, chromatin accessibility, binding of TFAP2A and of MITF, and the chromatin marks H3K27Ac and H3K27Me3 which are characteristic of active enhancers and silenced chromatin, respectively. Integrated analyses of these datasets indicate TFAP2 paralogs directly activate enhancers near genes enriched for roles in pigmentation and proliferation, and directly repress enhancers near genes enriched for roles in cell adhesion. Consistently, compared to WT cells, TFAP2-KO cells proliferate less and adhere to one another more. TFAP2 paralogs and MITF co-operatively activate a subset of enhancers, with the latter necessary for MITF binding and chromatin accessibility. By contrast, TFAP2 paralogs and MITF do not appear to co-operatively inhibit enhancers. These studies reveal a mechanism by which TFAP2 profoundly influences the set of genes activated by MITF, and thereby the phenotype of pigment cells and melanoma cells.

2022-04-26 | GSE190610 | GEO

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