Cell surface makeup of NECTIN1-deficient and proficient human melanoma cells in response to serum withdrawal
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Orbitrap Fusion Lumos
ORGANISM(S): Homo Sapiens (ncbitaxon:9606)
SUBMITTER: 
Julien Ablain
PROVIDER: MSV000090170 | MassIVE | Sat Aug 20 13:34:00 BST 2022
REPOSITORIES: MassIVE
Similar Datasets
Project description:Functional analysis of ABCB5 in A375 and G3361 melanoma cells, by comparing stably-transfected controls to ABCB5-shRNA-targeted cells. 12 samples total. Replicates n=3 for the following 4 groups: A375 pSUPER-retro-puro-Vector vs. A375 pSUPER-retro-puro-ABCB5-KD; G3361 pSUPER-retro-puro-shCNTRL vs. G3361 pSUPER-retro-puro-ABCB5-KD.
2014-06-17 | E-GEOD-38290 | biostudies-arrayexpress
Project description:Functional analysis of ABCB5 in A375 and G3361 melanoma cells, by comparing stably-transfected controls to ABCB5-shRNA-targeted cells.
2014-06-17 | GSE38290 | GEO
Project description:Using a chromatin regulator-focused shRNA library, we found that suppression of sex determining region Y-box 10 (SOX10) in melanoma causes resistance to BRAF and MEK inhibitors. To investigate how SOX10 loss leads to drug resistance, we performed transcriptome sequencing (RNAseq) of both parental A375 (Ctrl. PLKO) and A375-SOX10KD (shSOX10-1, shSOX10-2) cells. To ask directly whether SOX10 is involved indrug resistance in BRAF(V600E) melanoma patients, we isolated RNA from paired biopsies from melanoma patients (pre- and post- treatment) , that had gained BRAF or MEK inhibitor resistance . We performed RNAseq analysis to determine changes in transcriptome upon drug resistance.
2014-01-04 | GSE50535 | GEO
Project description:Using a chromatin regulator-focused shRNA library, we found that suppression of sex determining region Y-box 10 (SOX10) in melanoma causes resistance to BRAF and MEK inhibitors. To investigate how SOX10 loss leads to drug resistance, we performed transcriptome sequencing (RNAseq) of both parental A375 (Ctrl. PLKO) and A375-SOX10KD (shSOX10-1, shSOX10-2) cells. To ask directly whether SOX10 is involved indrug resistance in BRAF(V600E) melanoma patients, we isolated RNA from paired biopsies from melanoma patients (pre- and post- treatment) , that had gained BRAF or MEK inhibitor resistance . We performed RNAseq analysis to determine changes in transcriptome upon drug resistance. Investigate genes regulated by SOX10 and differntial gene expression between pre- and post-treatment biopsies. We use short hairpin RNA to suppression SOX10 in A375 cells and cells were harvested with trizol reagent for RNA isolation. For paired biopsies (patient samples) we collected the first biopsy before the initiation of treatment and the second biopsy after drug resistance developed. RNA was isolated from FFPE samples and subjected for RNA sequencing.
2014-01-04 | E-GEOD-50535 | biostudies-arrayexpress
Project description:We mapped the proteins secreted by A375 melanoma cells in the presence or absence of the PPARagonist rosiglitazone.
2019-02-18 | PXD009108 | Pride
Project description:We aimed to analyze the effects of Wnt-1 overexpression on the mRNA expression profile of human melanoma in a mouse xenograft model and correlated the results with then presence or absence of lymphangiogenesis and metastasis. Affymetrix gene expression analysis revealed activation of canonical and non-canonical targets genes in response to Wnt-1 as compared with controls. In regard to lymphangiogenic factors, the amount of VEGF-C was the single best marker to correlate with the amount of lymph-angiogenesis. mRNA expression array of human melanoma orthotopically grown in SCID mice. Comparison includes mRNA expression profile of two melanoma cell-lines (A375 and M24met) stably overexpressing control vector or Wnt-1 treated with or without CsA. Comparison #1 comprised Wnt-1 versus control in A375 and M24met melanoma, respectively. Comparison #2 comprised Wnt-1 + Cyclosporine A (CsA) versus Wnt-1 without CsA.
2012-06-04 | E-GEOD-26656 | biostudies-arrayexpress
Project description:Transcription factors, by acting on gene expression can affect molecular pathways and can thereby induce malignant transformation. Among the transcription factors involved in cellular transformation, we recently highlighted the role of RUNX2 in melanoma cell migration and proliferation. In the present study, we extended the analysis of the molecular effects of RUNT domain of RUNX2 in melanoma cells to deepen understanding of the underlying mechanisms. By the CRISPR/Cas9 system we generated the RUNT KO melanoma cells 3G8. Therefore, using a proteomic approach, we compared 3G8 with the original wild-type melanoma cell line (A375). The results showed a specific protein signature of 3G8 cells related to apoptosis and migration. In addition, proteomic analysis allowed us to point out the involvement of the RUNT domain in the neoangiogenesis process. Among the deregulated proteins implicated in angiogenesis we found fatty acid synthase, chloride intracellular channel protein-4, heat shock protein beta-1, Rho guanine nucleotide exchange factor 1, D-3-phosphoglycerate dehydrogenase, myosin-1c and caveolin-1. Accordingly, the VEGF gene expression was higher in A375 compared to 3G8 cells; HUVEC cells expressed increased levels of the neoangiogenetic markers CD105 and CD31 when co-cultured with A375 cells. In conclusion, our study provided new insight into RUNX2 molecular details which can be crucial to possibly propose it as an oncotarget of melanoma.
2019-11-13 | PXD012096 | Pride
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:Affymetrix microaaray analysis of healthy donor monocytes cultured for 64 hours in the absence of (culture monocytes), or presence of A375 cells (A375-MDSC) or treated with MIF inihibitor, 4-IPP (MDSC+4-IPP; 100mM, day 0 and 50mM, day 2).
2015-09-23 | GSE73333 | GEO
Project description:5 melanoma cell lines: MelJUSO, A375, 607B, 518A2, Skmel 28 Keywords: other
2004-10-19 | GSE1845 | GEO