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MTORC1 activation blocks BrafV600E-induced growth-arrest but is insufficient for melanoma formation

ABSTRACT: Expression profiling was performed using uncultured melanocytes and melanoma cell from various mouse models of BrafV600E induced melanocytic proliferation Various genotypes were analyzed at different time points in melanomagenesis RNA was purifired and hydridized to Affymetrix microarrays

ORGANISM(S): Mus musculus

SUBMITTER: William Damsky

PROVIDER: E-GEOD-61750 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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mTORC1 activation blocks BrafV600E-induced growth-arrest but is insufficient for melanoma formation

Project description:Expression profiling was performed using uncultured melanocytes and melanoma cell from various mouse models of BrafV600E induced melanocytic proliferation Various genotypes were analyzed at different time points in melanomagenesis

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Gene expression profile in melanomas from Pdk1-inactivated BrafV600E::Pten-/- mice

Project description:Gene expression profiling was performed to access the changes in gene expression in melanomas from Pdk1-inactivated Brafv600E::Pten-/- mice. The expression profiles of the BrafV600E::Pten-/-::Pdk1-/- were compared to the BrafV600E::Pten-/-::Pdk+/+ genotypes. The analysis has identified several important signaling pathways in Pdk1-dependent melanomagenesis. Melanoma tumors from the BrafV600E::Pten-/-::Pdk1+/+ and BrafV600E::Pten-/-::Pdk1-/- genotypes were harvested and mRNA from each group was pooled to enable four biologically replicates analysis.

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Gene expression profile in melanomas from Pdk1-inactivated BrafV600E::Pten-/- mice

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microRNAs Restrain Proliferation in BRAFV600E Melanocytic Nevi

Project description:microRNAs Restrain Proliferation in BRAFV600E Melanocytic Nevi

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mTORC1 activation blocks BrafV600E-induced growth arrest but is insufficient for melanoma formation.

Project description:Braf(V600E) induces benign, growth-arrested melanocytic nevus development, but also drives melanoma formation. Cdkn2a loss in Braf(V600E) melanocytes in mice results in rare progression to melanoma, but only after stable growth arrest as nevi. Immediate progression to melanoma is prevented by upregulation of miR-99/100, which downregulates mTOR and IGF1R signaling. mTORC1 activation through Stk11 (Lkb1) loss abrogates growth arrest of Braf(V600E) melanocytic nevi, but is insufficient for complete progression to melanoma. Cdkn2a loss is associated with mTORC2 and Akt activation in human and murine melanocytic neoplasms. Simultaneous Cdkn2a and Lkb1 inactivation in Braf(V600E) melanocytes results in activation of both mTORC1 and mTORC2/Akt, inducing rapid melanoma formation in mice. In this model, activation of both mTORC1/2 is required for Braf-induced melanomagenesis.

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UV irradiation or Lkb1 loss allows the identification of target genes preventing BRAFV600E-induced growth arrest in melanoma cells.

Project description:BRAFV600E-induced cell growth arrest in melanocytic nevus is on debate where only one third of melanomas arise directly from nevi. We showed that simultaneous neonatal oncogene (BRAFV600E) activation and UVB irradiation prevent BRafV600E-induced growth arrest in melanocytes, allowing melanoma development. A meta-analysis of gene expression profiles of melanocytes isolated from different mouse models and numerous studies revealed multiple common genes and processes involved in preventing BRafV600E-induced growth arrest. In humans, many of these genes are associated with poor survival and are upregulated during melanoma progression and in many RAS pathway activation-driven tumors. Single-cell profiling confirmed that BRAFV600E and the identified genes cooperate in melanocyte transformation, including the acquisition of multidrug resistance features. Depletion of these genes in vitro and in vivo revealed the utility of the encoded proteins as therapeutic targets. These results support the existence of BRAFV600E-mutated melanomas unassociated with nevus progression and identify targets for melanoma treatment

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microRNAs Restrain Proliferation in BRAFV600E Melanocytic Nevi [miRNA-Seq, RNA-Seq]

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Apoptosis, autophagy and senescence protect BRAFV600E nevi from malignant transformation

Project description:The oncogenic mutation BRAFV600E is a common event in nevi and melanomas, which are aggressive skin tumors characterized by MAPK signaling pathway activation. It has been observed that mutated benign melanocytic lesions can remain unchanged for decades, but also proliferate or undergo oncogene-induced senescence. The purpose of this study was to investigate the presence of a gene expression signature in BRAFV600E mutated nevi compared to wild-type ones, all derived from sun exposed sites. Microdissected tissues from excisional biopsies of acquired nevi were analyzed to detect the presence of BRAF and NRAS mutations and to profile whole genome expression by means of oligonucleotide microarrays. BRAFV600E mutation was evidenced in 64% of nevi, while no NRAS mutations were detected. Functional analysis of genes differentially expressed between wild-type and mutated lesions pointed out the role of oxidative stress in causing the oncogenic BRAF mutation and that the direct consequence of constitutive activation of BRAF-MEK-ERK pathway, in a benign contest, is the activation of apoptosis, autophagy and senescence. Our data also indicate that in mutated lesions, p53 plays a crucial role in the maintenance of the benign status.

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