Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA287912 | ENA |
REPOSITORIES: ENA
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Project description:Little is known about genes that promote melanoma cell growth and proliferation. siRNAs may be used to address the role of individual genesin these processes. RNAi library screens were used in the past to gain a comprehensive overview of all genes involved in cell growth, proliferation, migration and other cellular processes. A large-scale loss-of-function screen for eight different melanoma cell lines was performed using a pooled lentiviral shRNA library (GeneNet Human 50K lentiviral shRNA Library,cat#SI206B-1, System Biosciences) to identify genes relevant for melanoma cell growth and proliferation. shRNAs that lead to cell death or reduced growth of transduced melanoma cells are negatively selected and thereby underrepresented in the final cellular shRNA pool and vice versa. The shRNAs of the shRNA library (3-5 per gene) have complementary sequences to probes on the custom Affymetrix microarray HG-U133Plus2 and were analysed using this array. Well-known melanoma cell lines SK-Mel-103, A375, SK-Mel-147, SK-Mel-19, SK-Mel-28, SK-Mel-29, SK-Mel-5, WM3523cln6 were transduced with the lentiviral shRNA library and grown for 10 days under puromycin selection (day 10), control cells of respective cell lines were transduced and frozen immediately after transduction and genomic integration of shRNAs (day 0). Totel DNA was extracted and genomically integrated shRNAs were hybridized to Affymetrix microarrays (HG-U133Plus2.0 array).
2014-01-24 | E-GEOD-46675 | biostudies-arrayexpress
Project description:We report the six metastatic (RPMI-7951,SK-MEL-3,SH-4) and primary (A375,G-361,SK-MEL-1) melanoma cancer cells transcriptomics.
2021-03-14 | GSE162270 | GEO
Project description:Purpose. Aggressiveness is a crucial issue related to cutaneous melanoma malignancy and its high metastatic potential. Aim of this work is to identify new pathways or molecules controlling melanoma cell aggressiveness. Proliferation, migration and invasion capability under serum stimulation were analyzed in 12 human metastatic melanoma cell lines to identify the most aggressive ones as a model. The most proliferating/invading (defines as the most aggressive) A375 cell line was compared to the less aggressive one, Sk mel 28 by means of different approaches: 1) transcriptomic analysis by ILLUMINA platform; 2) proteomic study through LC-MS/MS analysis; 3) multiplexed assay to measure secretion of cytokines in conditioned media bioinformatic analysis was then carried out. Two groups of cells significantly differing in aggressiveness were identified and 2 cell lines, namely A375 and SK-Mel-28 were selected as model of the most and the less aggressive phenotype, respectively. A multi-omic analysis of several experimental datasets derived from transcriptomic, proteomic (mass spectrometric) and cytokinomic data was then carried out via Ingenuity Pathway Analysis (IPA) software. Analysis of upstream regulators and network analysis, indicated that the expression of tumor necrosis factor (TNF) were significantly differently expressed and functioning. The involvement of these pathways was confirmed by functional validation studies as zymography and proliferation studies and the most significantly upregulated pathway (TNF-alfa) was tested. Five melanoma cell lines with different MAGS were treated with an anti-TNFα monoclonal antibody and the most aggressive ones were highly significantly affected.
2019-01-08 | E-MTAB-4212 | biostudies-arrayexpress
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.
2014-04-20 | E-GEOD-42735 | biostudies-arrayexpress
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.
2014-04-20 | GSE42735 | GEO
Project description:Next Generation Sequencing in A375 and SK-MEL-28 cell lines
| PRJNA770917 | ENA
Project description:Aberrant DNA methylation and histone modifications both contribute to carcinogenesis, but how these two epigenetic factors interact to impact gene expression remain unclear. To address this issue, we studied gene expression profiles, DNA methylation and two key histone modifications (H3K4me3 and H3K27me3), in two types of normal melanocytes (HEMn and HEMa) and two melanoma cell lines SK-MEL-28 and LOXIMVI. Using these data, we analyzed the relationship between epigenetic factors and gene expression status in both normal and melanoma cells, and the impact of epigenetic switches on gene expression during melanomagenesis. ChIP-seq analysis of H3K4me3 and H3K27me3 in two types of normal melanocytes (HEMn and HEMa) and two melanoma cell lines (SK-MEL-28 and LOXIMVI).
2013-12-01 | E-GEOD-33930 | biostudies-arrayexpress
Project description:Analysis of transcriptome kinetics of SW1736 thyroid cancer cell line vs SK-MEL-28 melanoma cell line at various times after addition of 2 µM vemurafenib. The hypothesis tested was that SW1736 cells (vemurafenib-refractory) differentially express genes compared to SK-MEL-28 cells (vemurafenib sensitive) that confer resistance to the RAF inhibitor.
2013-02-01 | GSE37441 | GEO
Project description:Analysis of transcriptome kinetics of SW1736 thyroid cancer cell line vs SK-MEL-28 melanoma cell line at various times after addition of 2 µM vemurafenib. The hypothesis tested was that SW1736 cells (vemurafenib-refractory) differentially express genes compared to SK-MEL-28 cells (vemurafenib sensitive) that confer resistance to the RAF inhibitor. Total RNA was obtained from lysates of SW1726 and SK-MEL-28 cells treated with 2 µM vemurafenib for 0, 1, 6 and 48 h. Experiment was made by triplicate.
2013-02-01 | E-GEOD-37441 | biostudies-arrayexpress
Project description:Expression profiles of ADORA1-shRNA-transfected Sk-mel-28 human melanoma cell line and scrambled-shRNA control cells
2020-07-23 | GSE134493 | GEO