Project description:We have identified CUGBP1 dependent regulation of cell cycle and DNA replication/synthesis networks in melanoma cells. This data set we include gene expression and alternative splicing data of control and CUGBP1 depleted melanoma cell lines (SK-Mel-103 and UACC-62).
Project description:Purpose: Asess the transcritpional changes induced upon RAB7 knock-down in melanoma (SK-Mel-28 and UACC-62) and in colon cancer (HCT-116) cell lines. Methods: mRNA profiles of tumor cell lines (SK-Mel-28, UACC-62, HCT-116) stably expressing scrambled shRNA or RAB7 shRNA (harvested at day 3 after lentiviral infection) were generated by deep sequencing, using three biological replicates per condition. The sequence reads that passed quality filters were analyzed with TopHat and Cufflinks. Validation of induced / silenced genes was performed by western blot. Results show a differential impact of RAB7 expression in the transcriptomic profile of melanoma vs non-melanoma cell lines, and support a lineage-specific role of this small GTPase in melanoma.
Project description:Purpose: Assess the transcriptional changes induced upon RAB7 knock-down in melanoma (SK-Mel-28 and UACC-62) and in colon cancer (HCT-116) cell lines. Methods: mRNA profiles of tumor cell lines (SK-Mel-28, UACC-62, HCT-116) stably expressing scrambled shRNA or RAB7 shRNA (harvested at day 3 after lentiviral infection) were generated by deep sequencing, using three biological replicates per condition. The sequence reads that passed quality filters were analyzed with TopHat and Cufflinks. Validation of induced / silenced genes was performed by western blot. Results show a differential impact of RAB7 expression in the transcriptomic profile of melanoma vs non-melanoma cell lines, and support a lineage-specific role of this small GTPase in melanoma. Examination of the mRNA profiles RAB7-depleted vs wild type cells, performed in parallel in 3 different tumor cell lines (Melanomas: SK-Mel-28 and UACC-62, Non-melanoma: HCT-116) harvested at day 3 after lentiviral infection.
Project description:Melanoma is a genetically and phenotypically heterogeneous cancer, and changes in chromatin state have been implicated in melanoma progression, phenotypic plasticity, and tumor behavior. To investigate the epigenetic landscape associated with melanoma aggressiveness and mutational background, we performed ChIP-seq for the active chromatin mark H3K27ac and the repressive chromatin mark H3K9me3 in five human melanoma cell lines: SK-Mel-19, SK-Mel-29, SK-Mel-103, UACC-62, and UACC-257. These cell lines represent melanomas with different degrees of aggressiveness and distinct mutation profiles. Our analysis revealed differential patterns of H3K27ac across the cell lines, suggesting that enhancer-associated chromatin states are linked to mutation-dependent transcriptional regulation in melanoma.
