Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The gene regulation landscape of MTAP in lung adenocarcinoma

ABSTRACT: MTAP is an enzyme and found deleted in various cancers, but its role in lung adenoacrcinoma is still unclear. This study sought to investigate the effects of MTAP on the biological behavior and global gene expression profiles in lung adenocacinoma cells. We used expression microarrays to identify the global gene alterations in lung adenocacinoma cell line, CL1-5 cells after ectopically expressing V5-tagged MTAP gene.

ORGANISM(S): Homo sapiens

PROVIDER: GSE160522 | GEO | 2022/05/12

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

The gene regulation landscape of MTAP in lung adenocarcinoma

Project description:The gene regulation landscape of MTAP in lung adenocarcinoma

| PRJNA673435 | ENA

Expression Array analysis of MTAP in HT080 cells

Project description:Methylthioadenosine Phosphorylase (MTAP) is a tumor suppressor gene that encodes an enzyme responsible for the catabolism of the polyamine byproduct 5′deoxy-5′-methylthioadenosine (MTA). To elucidate the mechanism by which MTAP inhibits tumor formation, we have created isogenic MTAP+ and MTAP- HT1080 fibrosarcoma cells. In this experiment we have performed expression array analysis on MTAP-, MTAP+, and MTAP+ cells treated with the MTAP inhibitor MT-DADMe-ImmA. Three biological replicates of each sample were grown and analyzed. M- is MTAP-. M+ is MTAP+, and M+I is MTAP treated with inhibitor (48 hours).

2014-04-30 | E-GEOD-56112 | biostudies-arrayexpress

Expression Array analysis of MTAP in HT080 cells

2014-04-30 | GSE56112 | GEO

Repression of PRMT5-mediated dimethylation stabilizes vimentin and promotes metastasis in MTAP-loss lung cancer

Project description:Abstract The aggressive nature and poor prognosis of lung cancer led us to explore the mechanisms driving disease progression. Utilizing our invasive cell-based model, we identified methylthioadenosine phosphorylase (MTAP) and confirmed its suppressive effects on tumorigenesis and metastasis, and patients with low MTAP expression displayed worse overall and progression-free survival. Mechanistically, accumulation of methylthioadenosine substrate in MTAP-deficient cells reduced the level of protein arginine methyltransferase 5 (PRMT5)-mediated symmetric dimethylarginine (sDMA) modification on proteins. Vimentin was revealed as a novel dimethyl-protein with less dimethylation level in response to MTAP loss. The sDMA modification on vimentin reduces its protein abundance and trivially affects its filamentous structure. In MTAP-loss cells, lower sDMA level prevents ubiquitination-mediated vimentin degradation, thereby stabilizing vimentin, contributing to cell invasion. This inverse association of the MTAP/PRMT5 axis with vimentin proteins was clinically corroborated. Taken together, we propose a novel mechanism of vimentin post-translational regulation and provide new insights in metastasis.

2022-05-31 | PXD031192 | Pride

The gene regulation landscape of MITF in lung adenocarcinoma

Project description:MITF is a transcription factor and identified as a oncoprotein in melanoma, but its role in lung adenoacrcinoma is still unknown. This study sought to investigate the effects of MITF on the biological behavior and global gene expression profiles in lung adenocacinoma cells. We used expression microarrays to identify the global gene alterations in lung adenocacinoma cell line, CL1-0 cells after ectopic expressing three shRNA for knockdown MITF expression.

2023-03-12 | GSE146868 | GEO

MRTX1719 is an MTA-cooperative PRMT5 inhibitor that exhibits synthetic lethality in preclinical models and patients with MTAP deleted cancer

Project description:Previous studies implicated PRMT5 as a synthetic lethal target for MTAP deleted (MTAP del) cancers, however, the pharmacological characterization of small molecule inhibitors that recapitulate the synthetic lethal phenotype have not been described. MRTX1719 selectively inhibited PRMT5 in the presence of MTA, which is elevated in MTAP del cancers, and inhibited PRMT5-dependent activity and cell viability with >70-fold selectivity in HCT116 MTAP del compared to HCT116 MTAP WT cells. MRTX1719 demonstrated dose-dependent anti-tumor activity and inhibition of PRMT5-dependent SDMA modification in MTAP del tumors. In contrast, MRTX1719 demonstrated minimal effects on SDMA and viability in MTAP WT tumor xenografts, mouse or human hematopoietic cells. MRTX1719 demonstrated marked anti-tumor activity across a panel of xenograft models at well-tolerated doses. Early signs of clinical activity were observed including objective responses in patients with MTAP del melanoma, gallbladder adenocarcinoma, mesothelioma, non-small cell lung cancer, and MPNST from the Phase 1/2 study. Significance: PRMT5 was identified as a synthetic lethal target for MTAP del cancers, however, previous PRMT5 inhibitors do not selectively target this genotype. The differentiated binding mode of MRTX1719 leverages the elevated MTA in MTAP del cancers and represents a promising therapy for the ~10% of cancer patients with this biomarker.

2023-08-09 | GSE240145 | GEO

MTAP loss promotes stemness and epigenetic reprogramming in Glioblastoma

Project description:Methylthioadenosine Phosphorylase (MTAP) loss is one of the most frequent genetic alterations in Glioblastoma and has been associated with poor clinical outcomes in several cancer types. Here we used patient derived glioblastoma cell lines and manipulated MTAP status to create isogenic pairs with which to study the effects of this alteration on epigenetics, gene expression, and cell identity

2019-11-01 | GSE130093 | GEO

Of eyes and embryos; subfunctionalization of the CRX homeobox gene in mammalian evolution

Project description:We have ectopically expressed two V5-tagged homeobox genes and a control plasmid in mouse embryonic fibroblasts. Following ectopic expression and chemical selection we used whole transcriptome sequencing to reveal any effect of forced missed expression on the MEF transcriptome.

2020-04-13 | GSE129456 | GEO

Mouse Obox and CrxOS modulate pre-implantation transcriptional profiles revealing similarity between paralogous mouse and human homeobox genes

Project description:We have ectopically expressed four V5-tagged mouse homeobox genes in mouse embryonic fibroblasts with endogenous expression restricted to the preimplantation mouse embryo. Following ectopic expression we used whole transcriptome sequencing to reveal any effect of forced missed expression on the MEF transcriptome.

2018-02-22 | GSE108060 | GEO

MicroRNA-449a Enhances Radiosensitivity in Lung Adenocarcinoma Cells

Project description:Twenty-five miRNAs were identified as having differential expression post-irradiation in CL1-0 or CL1-5 cells. Among these miRNAs, miR-449a, which was down-regulated in CL1-0 cells at 24 h after irradiation, was chosen for further investigation. Overexpression of miR-449a in CL1-0 cells effectively increased irradiation-induced DNA damage and apoptosis, altered the cell cycle distribution and eventually led to sensitization of CL1-0 to irradiation. MiR-449a might be a novel radiosensitizer for clinical applications. Two lung adenocarcinoma cell lines (CL1-0 and CL1-5) with different metastatic ability and radiosensitivity were used. In order to understand the regulatory mechanisms of differential radiosensitivity in these isogenic tumor cells, both CL1-0 and CL1-5 were treated with 10 Gy radiation, and were harvested respectively at 0, 1, 4, and 24 h after radiation exposure. The changes in expression of miRNA upon irradiation were examined using Illumina Human microRNA BeadChips.

2012-12-30 | E-GEOD-40602 | biostudies-arrayexpress

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