Expression data from invasive melanoma cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA471248 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data of BRAF inhibitor resistant melanoma cells
| PRJNA471347 | ENA
Project description:Expression data from second oncogene expressing Melanoma Cells.
| PRJNA506456 | ENA
Project description:Melanoma is a very aggressive type of skin cancer, which renders it difficult to treat because of extensive heterogeneity frequently observed in melanoma tumours. Here we hypothesized that gene expression and DNA methylation differences would correlate with invasiveness in melanoma cells. To address this question, we carried out genome-wide transcriptome and methylome investigations in non-invasive and invasive groups of melanoma cell lines.
2021-04-06 | GSE153594 | GEO
Project description:Melanoma is a very aggressive type of skin cancer, which renders it difficult to treat because of extensive heterogeneity frequently observed in melanoma tumours. Here we hypothesized that gene expression and DNA methylation differences would correlate with invasiveness in melanoma cells. To address this question, we carried out genome-wide transcriptome and methylome investigations in non-invasive and invasive groups of melanoma cell lines.
2021-04-06 | GSE153592 | GEO
Project description:Melanoma is the deadliest form of skin cancer, due to its tendency to metastasize early. Brother of Regulator of Imprinted Sites (BORIS), also known as CCCTC binding factor-Like (CTCFL), is a transcription regulator that becomes ectopically expressed in melanoma. We recently showed that BORIS contributes to melanoma phenotype switching by altering the gene expression program of proliferative melanoma cells in favor of a more invasive phenotype. However, how BORIS alters the transcriptome remains unclear. Here, ATAC-seq was used to study BORIS-mediated chromatin accessibility alterations in proliferative melanoma cells. Genes that gained promoter accessibility following ectopic BORIS expression, were enriched for melanoma-specific invasive genes as well as invasion-associated biological processes, while promoters of genes associated with proliferation show reduce accessibility. Integration of ATAC-Seq and RNA-Seq data demonstrates that increased chromatin accessibility is associated with transcriptional upregulation of genes involved in tumor progression processes, and the aberrant activation of oncogenic transcription factors, while reduced chromatin accessibility and downregulated genes, were associated with repressed activity of tumor suppressors. Together, these findings indicate that BORIS mediates transcriptional reprogramming in melanoma cells by altering chromatin accessibility and gene expression, shifting the cellular transcription landscape of proliferative melanoma cells towards a pro-invasive genetic signature.
2023-04-21 | GSE211800 | GEO
Project description:Melanoma cell lines were established and used for Affymetrix Human Gene 1.0 ST Array
2019-10-20 | GSE114380 | GEO
Project description:Expression data from A375 melanoma parental and persister cells
| PRJNA566397 | ENA
Project description:Dissection of melanoma heterogeneity through gene expression profiling has led to the identification of two major phenotypes, conventionally defined as “MITF high / proliferative” and “AXL high / invasive”. Tumors or single melanoma cells characterized by a predominant AXL-related gene program show enhanced expression of sets of genes involved in motility, invasion and regulation of epithelial-mesenchymal transition (EMT), while these genes are downregulated in tumors or cells with a predominant MITF-related gene program. The activation of the AXLhi/MITFlo invasive gene program in melanoma is characterized by aberrant expression of transcription factors (TFs) involved in the embryonic EMT process. Additional master genes involved in promoting melanoma growth and invasive state have been identified within the family of epigenetic regulators. Two of these genes, RNF2 and EZH2, components of the polycomb repressive complexes 1 and 2, act by epigenetically silencing tumor suppressors that in turn regulate the invasive and EMT-like phenotype of melanoma cells. Additional master genes involved in promoting melanoma growth and invasive state have been identified within the family of epigenetic regulators. Two of these genes, RNF2 and EZH2, components of the polycomb repressive complexes 1 and 2, act by epigenetically silencing tumor suppressors that in turn regulate the invasive and EMT-like phenotype of melanoma cells. Here we provide evidence for a new actionable pathway that controls melanoma EMT-like/invasive phenotype. We show that in MITFlo melanomas, the TF NFATc2 controls the EMT-like transcriptional program, the invasive ability of neoplastic cells, as well as in-vitro and in-vivo growth, through a pathway that functionally links c-myc to FOXM1 and EZH2. Targeting of NFATc2, FOXM1 or EZH2 inhibited melanoma migratory and invasive activity. Moreover, pharmacological co-targeting of NFATc2 and EZH2 promoted apoptosis of BRAF-mutant melanomas with intrinsic resistance to BRAF inhibition.
2019-02-06 | GSE101323 | GEO
Project description:The epigenetic regulator BMI1 is upregulated in many human malignancies and has been implicated in cell migration, but the impact on autochthonous tumor progression is unexplored. Our analyses of human expression data show that BMI1 levels increase with progression in melanoma. We find that BMI1 expression in melanoma cells does not influence cell proliferation or primary tumor growth. In contrast, BMI1 levels are a key determinant of melanoma metastasis, whereby deletion impairs and overexpression enhances dissemination. Remarkably, BMI1’s pro-metastatic effect reflects enhancement of all stages of the metastatic cascade including invasion, migration, extravasation, adhesion and survival. Additionally, downregulation or upregulation of BMI1 induces sensitivity or resistance to BRAF inhibitor. Consistent with these pleiotropic effects, we find that BMI1 promotes widespread gene expression changes that encompass key hallmarks of the melanoma invasive signature, including activation of TGFβ, non-canonical Wnt, EMT and EGF/PDGF pathways. Importantly, for both primary and metastatic melanoma samples, this BMI1-induced signature identifies invasive subclasses of human melanoma and predicts poor patient outcome. Our data yield key insights into melanoma biology and establish BMI1 as a compelling drug target whose inhibition would suppress both metastasis and chemoresistance.
2016-02-03 | GSE71890 | GEO
Project description:Understanding the molecular processes underlying intra-tumor heterogeneity is of critical importance to improve the efficiency of therapy and overcome drug resistance. In malignant melanoma, heterogeneity is though to arise -at least partly- through epigenetic rather than genetic reprogramming of proliferating cells, leading to the appearance within the primary tumors of a phenotypically distinct invasive cell subpopulation. The invasive melanoma cells are at the origin of metastatic spread and are thought to provide a reservoir of therapeutically resistant cells. To decipher the gene regulatory networks that underlie the proliferative and invasive cellular states we integrated publicly available gene expression and DNA methylation data from tumor biopsies with a newly generated compendium of open chromatin and histone modification profiling of melanoma cultures that are dominant in either of the two subpopulations. Extensive in silico analyses identified SOX10 and MITF, and AP-1 and TEADs as key upstream regulators of the proliferative and invasive transcriptomes, respectively. Knock-down experiments confirmed the implication of TEADs in the invasive gene network and, more importantly, established a causative link between activation of these transcription factors and melanoma cell invasion and sensitivity to MAPK inhibitors.
2015-03-05 | GSE60664 | GEO