B16F1-ACT-EDT
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB46156 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cancer patients after successful therapy contain nested in their organs and/or circulating in the systemic fluids tumor cells that remain asymptomatic for an extended period of time. They stay dormant with no apparent immediate potential to develop into a clinically manifested tumor until activated by yet not well defined mechanisms. We previously developed tumor dormancy model of murine melanoma, a cancer with a high potential of phenotype plasticity to adapt to micro-environmental changes, in which to investigate cellular quiescence and related factors as a potential mechanism of tumour dormancy. In this study, to explore molecular mechanism responsible for cellular dormancy, we performed a comparative transcriptome analysis of dormant B16F1-GFP-D and derived dormant brain metastasis (DB) with maternal B16F1-GFP-M cells.
2024-09-13 | GSE250145 | GEO
Project description:B16F1 cells are a good model to study cell motility and cytoskeletal organization. In our lab, a combination of microscopy and gene silencing was used to approach the problem. Having gene expression profiles for B16F1 would facilitate and support subsequent gene silencing by RNAi as well as potentially identify new molecular players. We used microarrays to detail the expression profiles in cells cultured in regular conditions. These profile will serve as a reference point for further studies. Experiment Overall Design: Three biological replicats of control untreated B16F1 mouse melanoma cells were processed on mouse GeneChip arrays 430A. Reliability, variability, and reprodusibility of data generated by microarrays were addressed.
2008-06-13 | E-GEOD-4819 | biostudies-arrayexpress
Project description:B16F1 cells are a good model to study cell motility and cytoskeletal organization. In our lab, a combination of microscopy and gene silencing was used to approach the problem. Having gene expression profiles for B16F1 would facilitate and support subsequent gene silencing by RNAi as well as potentially identify new molecular players. We used microarrays to detail the expression profiles in cells cultured in regular conditions. These profile will serve as a reference point for further studies. Keywords: control
2006-09-27 | GSE4819 | GEO
Project description:Comparison of transcriptomic profile of the murine B16F1-GFP-M melanoma cells with the derived dormant B16F1-GFP-D, B16F1-GFP-DB#1, B16F1-GFP-DB#2, B16F1-GFP-DB#3 melanoma cells
| PRJNA1052105 | ENA
Project description:Purpose: to evaluate changes in the expression of microRNAs, which contribute to explain a phenotype of differential pigmentation and reduction of proliferation, in B16F1 melanoma cells exposed to analogue of tymidine BrdU or aminoacid L-Tyr Methods: Small RNAseq evaluation of the expression profiles of miRNAs in B16F1 melanoma cells exposed to BrdU (0.25 μg / mL) and L-Tyr (5 mM) for 72 h, as well as the expression by RT-qPCR of some molecular targets related with melanogenesis, cell cycle and senescence and construction of network models of regulation and co-expression of microRNAs. Results: It was confirmed that stimulation or melanogenic repression with L-Tyr or BrdU, respectively, generates changes in melanin concentration, reduction in proliferation and changes in expression of microRNAs 470-3p, 470-5p, 30d-5p , 129-5p, 148b-3p, 27b-3p and 211-5p, which presented patterns of coordinated co-expression, related to melanogenesis through their putative targets MITF, Tyr and Tyrp1 and control of cell cycle and senescence: Cyclin D1, Cdk2, Cdk4 and p21. Conclusion: This work improves our understanding of the events of melanogenesis, cell cycle control, and senescence mediated by the coordinated expression of miRNAs and helps to develop new approaches to a molecular biology of melanoma that operates in network
2020-03-19 | GSE147170 | GEO
Project description:Mouse melanomas treated with epitope-standardized adoptive T-cell therapy targeting different endogenous gene products
| PRJEB30997 | ENA
Project description:Mouse melanomas treated with epitope-standardized adoptive T cell therapy targeting endogenously encoded melanosomal RAB38
| PRJEB37461 | ENA
Project description:Cancer patients after successful therapy contain nested in their organs and/or circulating in the systemic fluids tumor cells that remain asymptomatic for an extended period of time. They stay dormant with no apparent immediate potential to develop into a clinically manifested tumor until activated by yet not well defined mechanisms. In the present study, we developed tumor dormancy model of murine melanoma, a cancer with a high potential of phenotype plasticity to adapt to micro-environmental changes, in which to investigate cellular quiescence and related factors as a potential mechanism of tumour dormancy. To explore molecular mechanism responsible for cellular dormancy, we performed a comparative transcriptome analysis of dormant B16F1-GFP-D and maternal B16F1-GFP-M cells. Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a nuclear receptor highly expressed by colonic epithelial cells. It plays a key role in gut homeostasis and metabolism regulation. We previously showed that PPARgamma has a role in the action of aminosalycilates (5-ASA), one of the oldest anti-inflammatory agents used in the treatment of inflammatory bowel disease. These data have prompted us to develop novel analogues of 5-ASA with greater PPARgamma-activating properties (GED). The various PPARgamma ligands appear to have some markedly different effects, some of which can induce adverse effects. The transcriptomic profiles induced by various families of PPARgamma ligands are very poorly known and especially in intestinal epithelial cells. Hence, the objectives of the present project are to compare the gene expression profile induced by GED, 5-ASA, and pioglitazone in Caco-2 cells, in order to better understand these compounds’ modes of action, to discover potential new PPARgamma target genes in intestinal epithelial cells and to explain the efficacy difference between GED and 5-ASA.
2017-02-14 | GSE69703 | GEO
Project description:Triggering of cAMP and mitogen-activated (MAPK) pathways in response to hormonal and growth factor cues promotes melanocyte pigmentation and survival in part through induction of the master regulator MITF by cAMP-responsive factor CREB. We examined the role of CREB coactivators (CRTC1-3) in transduction of cAMP and MAPK signals in melanocytes. We found that CRTC3 knock-out in mice and B16F1 melanoma cells decreases pigmentation by directly regulating the expression of the melanosomal transporter OCA2. In addition to effects of cAMP, CRTC3 activation was also promoted by ERK1/2-mediated phosphorylation at Ser391; amounts of phosphorylated CRTC3-S391 were constitutively elevated in human melanoma cells expressing mutated BRAF or NF1. Knock-out of CRTC3 in A375 melanoma cells impaired their anchorage-independent growth, migration and invasiveness, whereas CRTC3 over-expression increased survival in response to BRAF inhibition by vemurafenib. Analysis of spontaneous CRTC3 mutations in melanomas reveals that increased activity of this co-activator associates with reduced patient survival. Our results highlight the importance of CRTC3 in pigmentation and melanoma progression.
2022-04-12 | GSE154116 | GEO
Project description:Triggering of cAMP and mitogen-activated (MAPK) pathways in response to hormonal and growth factor cues promotes melanocyte pigmentation and survival in part through induction of the master regulator MITF by cAMP-responsive factor CREB. We examined the role of CREB coactivators (CRTC1-3) in transduction of cAMP and MAPK signals in melanocytes. We found that CRTC3 knock-out in mice and B16F1 melanoma cells decreases pigmentation by directly regulating the expression of the melanosomal transporter OCA2. In addition to effects of cAMP, CRTC3 activation was also promoted by ERK1/2-mediated phosphorylation at Ser391; amounts of phosphorylated CRTC3-S391 were constitutively elevated in human melanoma cells expressing mutated BRAF or NF1. Knock-out of CRTC3 in A375 melanoma cells impaired their anchorage-independent growth, migration and invasiveness, whereas CRTC3 over-expression increased survival in response to BRAF inhibition by vemurafenib. Analysis of spontaneous CRTC3 mutations in melanomas reveals that increased activity of this co-activator associates with reduced patient survival. Our results highlight the importance of CRTC3 in pigmentation and melanoma progression.
2022-04-12 | GSE154115 | GEO