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Transcriptionally inactive ATF2 variant drives melanomagenesis

ABSTRACT: Transcriptionally inactive ATF2 variant drives melanomagenesis

PROVIDER: PRJNA320278 | ENA |

REPOSITORIES: ENA

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Transcriptionally inactive ATF2 variant drives melanomagenesis [Seq]

Project description:Characterized by striking metastatic propensity and chemoresistance, melanoma is among the most lethal cutaneous malignancies. The transcription factor ATF2 was shown to elicit oncogenic activities in melanoma, and its inhibition attenuates melanoma development. Here, a mouse model engineered to express a transcriptionally inactive form of Atf2 (Atf2?8,9) was found to be sufficient to induce nevi formation and, when crossed with BrafV600E animals, to promote melanoma development. The cross of Atf2?8,9 with BrafV600E;Pten-/- mice augmented pigmentation, tumorigenicity, and metastasis. Similar to mouse Atf2?8,9, the human ATF2 splice variant 5 enhanced growth and migration capacity of cultured melanoma and immortalized melanocytes. Induced Melan-A, CXCL9, S100A8, CCR7 expression, seen in Atf2?8,9-driven tumors associate with their enhanced pigmentation, immune infiltration and propensity to metastasize. Notably, elevated ATF2SV5 expression in melanoma specimens coincided with poor prognosis. The gain-of-function activity elicited by the truncated ATF2 form offers unexpected insight into mechanisms underlying melanoma development and progression.

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Transcriptionally inactive ATF2 variant drives melanomagenesis [Array]

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A Transcriptionally Inactive ATF2 Variant Drives Melanomagenesis.

Project description: Not available

| S-EPMC4889472 | biostudies-literature

Mus musculus

Project description:Transcriptionally inactive ATF2 variant drives melanomagenesis [Array]

| PRJNA320281 | ENA

Homo sapiens

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Transcriptionally inactive ATF2 variant drives melanomagenesis

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

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Regulation of gene expression by ATF2 in mouse melanocytes

Project description:primary melanocytes from WT and ATF2 mutant (transcriptionally inactive) mice expressing the mutant N-ras transgene were prepared and assessed for changes in gene expression when maintained under normoxia and hypoxia growth conditions. 12 mouse melanocyte samples were analyzed during normoxia and hypoxia, with different ATF2 genotypes. The pivotal samples are represented as duplicates. Treatment of tamoxifen was used to induce recombination and expression of the mutant ATF2 (inducible Cre). Doxycyclin was used to induce expression of mutant N-Ras transgene.

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