Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling following the overexpression or the knockdown of Ambra1 in A375 melanoma cell lines

ABSTRACT: Melanoma is the most deadly type of skin cancers and, there is a continuous need to develop early biomarkers as well as treatments to improve the survivability of patients. Ambra1 is an essential regulator in autophagy and it has been recently shown to have a role in cell proliferation. We used microarrays to analyse the transcriptomic changesi n A375 melanoma cell lines following Ambra1 differential expression

ORGANISM(S): Homo sapiens

PROVIDER: GSE175361 | GEO | 2021/05/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Targeting cancer stem cells in medulloblastoma by inhibiting AMBRA1 dual function in autophagy and STAT3 signalling

Project description:Medulloblastoma (MB) is a childhood malignant brain tumour comprising four main subgroups characterized by different genetic alterations and rate of mortality. Among MB subgroups, patients with enhanced levels of the c-MYC oncogene (MBGroup3) have the poorest prognosis. Here we identified a previously unrecognized role of the pro-autophagy factor AMBRA1 in regulating MB. We demonstrated that AMBRA1 expression levels strongly depend on c-MYC expression and correlate with patient poor prognosis; also, knockdown of AMBRA1 reduces MB stem potential, growth and migration of MBGroup3 cells in vitro and in vivo. At a molecular level, AMBRA1 mediates these effects by suppressing SOCS3, an inhibitor of STAT3 activation. In turn, active STAT3 increases c-MYC expression that, in a positive feedback loop, sustains AMBRA1 transcription. Importantly, pharmacological inhibition of autophagy profoundly affects stem potential and metastasization of MBGroup3 cells in vitro and in vivo, and a combined anti-autophagy and anti-STAT3 approach impacts MBGroup3 cell survival. Taken together, our data identified the c-MYC/AMBRA1/STAT3 axis as a strong oncogenic signalling pathway with significance for both patient stratification strategies and targeted treatments of MBGroup3.

2021-09-08 | GSE134109 | GEO

Effect of IMD-0354 on gene expression in melanoma A375 cells

Project description:The purpose of this RNAseq is to analyse the effect of compound IMD-0354 on gene expression in melanoma A375 cells. RNAseq analysis identified unfolded protein response, cell cycle and DNA damage pathways to be effected by IMD-0354.

2021-02-02 | GSE165899 | GEO

Transcriptome profile of melanoma cell lines A375 and A375-BIR (BIR-BRAF INHIBITOR RESISTANT) during dabrafenib treatment

Project description:To analyse gene expression differences between A375 and A375-BIR during the treatment with dabrafenib (DAB)

2022-08-29 | GSE165334 | GEO

SmallRNAome profile of melanoma cell lines A375 and A375-BIR (BIR-BRAF INHIBITOR RESISTANT) during dabrafenib treatment

Project description:To analyse smallRNA expression differences between A375 and A375-BIR during the treatment with dabrafenib (DAB)

2024-05-03 | GSE165335 | GEO

Gene expression profiling following the overexpression or the knockdown of Ambra1 in A375 melanoma cell lines

Project description:Gene expression profiling following the overexpression or the knockdown of Ambra1 in A375 melanoma cell lines

| PRJNA732077 | ENA

The AMBRA1 E3 ligase adaptor regulates the stability of cyclin D

Project description:The initiation of cell division integrates a large number of intra- and extracellular inputs. D-type cyclins (hereafter, cyclin D) couple these inputs to the initiation of DNA replication1. Increased levels of cyclin D promote cell division by activating cyclin-dependent kinases 4 and 6 (hereafter, CDK4/6), which in turn phosphorylate and inactivate the retinoblastoma tumour suppressor. Accordingly, increased levels and activity of cyclin D-CDK4/6 complexes are strongly linked to unchecked cell proliferation and cancer2,3. However, the mechanisms that regulate levels of cyclin D are incompletely understood4,5. Here we show that autophagy and beclin 1 regulator 1 (AMBRA1) is the main regulator of the degradation of cyclin D. We identified AMBRA1 in a genome-wide screen to investigate the genetic basis of the response to CDK4/6 inhibition. Loss of AMBRA1 results in high levels of cyclin D in cells and in mice, which promotes proliferation and decreases sensitivity to CDK4/6 inhibition. Mechanistically, AMBRA1 mediates ubiquitylation and proteasomal degradation of cyclin D as a substrate receptor for the cullin 4 E3 ligase complex. Loss of AMBRA1 enhances the growth of lung adenocarcinoma in a mouse model, and low levels of AMBRA1 correlate with worse survival in patients with lung adenocarcinoma. Thus, AMBRA1 regulates cellular levels of cyclin D, and contributes to cancer development and the response of cancer cells to CDK4/6 inhibitors.

2021-02-04 | GSE146303 | GEO

Whole Exome PC9 and A375

Project description:Drug resistant population of PC9(human non-small cell lung cancer) or A375 (human melanoma) cell lines were used for this study. By exome sequencing, we will analyse mutations of cells in drug tolerent state and after drug holiday.

| EGAS00001002493 | EGA

A four-arm study of A375 melanoma cell line-derived xenograft tumors in NSG mice treated with Vemurafenib and CB839

Project description:Melanoma is a rare but deadly form of skin cancer, which is often treated with BRAF inhibitors such as Vemurafenib (referred to as PLX4032). Whilst Vemurafenib prolongs the survival of patients, BRAF inhibitor resistance inevitably occurs in most cases. Previous studies demonstrated that metabolic rewiring occurs in BRAF inhibitor resistance and causes dependence on glutamine. To investigate whether this vulnerability could be exploited with clinically relevant drugs, we used the BRAF inhibitor, Vemurafenib, and the glutaminase imhibitor, CB839 to treat A375-derived melanoma xenografted tumors. We showed that whilst CB839 did not significantly affect the growth of A375-derived tumors compared to those given a vehicle, the addition of CB839 to Vemurafenib treatment had a significant anti-tumor effect. Tumors were taken at the endpoint (Max tumor length 15mm) from the 6 mice in each treatment group and cut into fragments and stored in RNAlater for RNAseq analysis. RNA extraction was performed on 1-3 fragments per tumor to make up 200-300mg of tissue.

2023-04-07 | E-MTAB-12811 | biostudies-arrayexpress

Expression data from A375 melanoma parental and persister cells

Project description:Identify transcriptionnally and translationally regulated mRNA in melanoma parental and persister cells In this dataset, we include expression data of A375 melanoma drug-naïve parental cells and A375 melanoma persister cells that survived from BRAF and MEK inhibition. The expression data are studied in both total RNA and polysome-bounded RNA.

2019-09-20 | GSE137724 | GEO

Gene expression profiling of isogenic malignant melanoma A375-BRAFV600E/NRASQ61 and A375-BRAFV600E/NRASQ61K cell lines

Project description:BRAF-inhibitor (BRAFi)-resistance compromises long term survivorship of malignant melanoma patients, and mutant NRAS is a major mediator of BRAFi-resistance. We have employed NanoString nCounterTM transcriptomic analysis of isogenic human malignant melanoma cells that differ only by NRAS mutational status (BRAFi-sensitive A375-BRAFV600E/NRASQ61 versus BRAFi-resistant A375-BRAFV600E/NRASQ61K), identifying modulation of specific gene expression networks as a function of NRASQ61K-status.

2021-09-23 | GSE184633 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data