Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ALKBH5 facilitates the progression of skin cutaneous melanoma through promoting ABCA1 demethylation and inhibiting autophagy in an m6A-dependent manner

ABSTRACT: ALKBH5 facilitates the progression of skin cutaneous melanoma through promoting ABCA1 demethylation and inhibiting autophagy in an m6A-dependent manner

PROVIDER: PRJNA1067136 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27668425_1.fastq.gz	Fastqsanger.gz
	SRR27668425_2.fastq.gz	Fastqsanger.gz
	SRR27668426_1.fastq.gz	Fastqsanger.gz
	SRR27668426_2.fastq.gz	Fastqsanger.gz
	SRR27668427_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

ALKBH5 facilitates the progression of skin cutaneous melanoma through promoting ABCA1 demethylation and inhibiting autophagy in an m6A-dependent manner

Project description:Background: N6-methyladenosine (m6A) is the most common and abundant mRNA modification, playing an essential role in biological processes and tumor development. However, the role of m6A methylation in skin cutaneous melanoma (SKCM) is not yet clear. This study analyzed the expression of m6A-related functional genes in SKCM and aimed to explore the key demethylase ALKBH5 mediated m6A modification and its potential mechanism in human SKCM. Methods: Based on public databases, the m6A-related gene expression landscape in SKCM was portrayed. MeRIP-Seq and RNA-Seq were used to recognize the downstream target of ALKBH5. In vivo and in vitro functional phenotype and rescue functional experiments were performed to explore the mechanism of the ALKBH5-ABCA1 axis in SKCM. Results: We found ALKBH5 upregulated in SKCM, associated with poor prognosis. ALKBH5 can promote melanoma cell proliferation, colony formation, migration, and invasion and inhibit autophagy in vitro, facilitating tumor growth and metastasis in vivo. We identified ABCA1, a membrane protein that assists cholesterol efflux, as a downstream target of ALKBH5-mediated m6A demethylation. Finally, our data demonstrated that ALKBH5 promoted SKCM via mediating ABCA1 downregulation by reducing ABCA1 mRNA stability in an m6A-dependent manner. Conclusion: Our findings exhibited the functional value of the key demethylase ALKBH5 mediated m6A modification in the progression of SKCM, suggesting ALKBH5 and its target ABCA1 as potential therapeutic targets in SKCM.

2024-02-29 | GSE253795 | GEO

ALKBH5-mediated m6A demethylation ameliorates extracellular matrix deposition in cutaneous pathological fibrosis

Project description:ALKBH5-mediated m6A demethylation ameliorates extracellular matrix deposition in cutaneous pathological fibrosis

| PRJNA1102882 | ENA

ALKBH5 facilitates the progression of skin cutaneous melanoma via mediating ABCA1 demethylation and modulating autophagy in an m6A-dependent manner

Project description: Not available

| S-EPMC10929202 | biostudies-literature

ALKBH5-mediated m6A demethylation ameliorates extracellular matrix deposition in cutaneous pathological fibrosis [meRIP-seq]

Project description:ALKBH5-mediated m6A demethylation ameliorates extracellular matrix deposition in cutaneous pathological fibrosis [meRIP-seq]

| PRJNA1104121 | ENA

ALKBH5 is a New Mammalian RNA Demethylase

Project description:N6-methyladenosine (m6A) is the most prevalent internal modification of messenger RNA (mRNA) in higher eukaryotes. Here we report ALKBH5 as a new mammalian demethylase that oxidatively removes the m6A modification in mRNA in vitro and inside cells. This demethylation activity of ALKBH5 significantly affects mRNA export and RNA metabolism as well as the assembly of mRNA processing factors in nuclear speckles. Alkbh5-deficient male mice are characterized by impaired fertility resulting from apoptosis that affects meiotic metaphase-stage spermatocytes. In accordance with this defect, we have identified in mouse testes 1552 differentially expressed genes which cover broad functional categories and include spermatogenesis-related mRNAs involved in the p53 functional interaction network. We show that Alkbh5-deficiency impacts the expression levels of some of these mRNAs, supporting the observed phenotype. The discovery of this new RNA demethylase strongly suggests that the reversible m6A modification plays fundamental and broad functions in mammalian cells. RNA-seq in two cell types

2013-02-15 | E-GEOD-40132 | biostudies-arrayexpress

ALKBH5-mediated m6A demethylation ameliorates extracellular matrix deposition in cutaneous pathological fibrosis

Project description:Hypertrophic scars (HTS) are fibrotic skin disorders characterized by excessive deposition of dermal extracellular matrix (ECM), presenting significant challenges in clinical management despite incomplete understanding of their underlying mechanisms. Using MeRIP-seq and RNA-seq, our study initially revealed the direct regulatory role of ALKBH5 on ECM components in dermal fibroblasts, thereby involving in the pathogenesis of HTS.

2024-09-13 | GSE264515 | GEO

ALKBH5-mediated m6A demethylation ameliorates extracellular matrix deposition in cutaneous pathological fibrosis [meRIP-seq]

2024-09-13 | GSE264743 | GEO

ALKBH5 regulates paclitaxel resistance in NSCLC via inhibiting CEMIP-mediated EMT

Project description:N6-methyladenosine (m6A) is the most printed and prevalent mRNA modification, which was verified to be closely correlated with cancer occurrence and progression. As m6A demethlyase, the dysregulation of ALKBH5 was observed in various cancer. However, the role and underlying machinery of ALKBH5 in NSCLC pathogenesis, especially the chemo-resistance was poorly elucidated. The current study indicated that ALKBH5 was decreased during paclitaxel (PTX) resistant process and its down-regulation usually implied poor prognosis of NSCLC patients. Over-expression of ALKBH5 in PTX-resistant cells could suppressed cell proliferation and enhanced chemo-sensitivity. Whereas, knockdown of ALKBH5 exerted opposite effect, which further supported the tumor suppressive role of ALKBH5. Over-expression of ALKBH5 also could reverse the EMT process in PTX-resistant cancer cells. Mechanistically, data of RNA-seq, Real-time PCR and western blotting indicted that CEMIP, also known as KIAA1199, may be the downstream target of ALKBH5. And ALKBH5 could negatively regulated the CEMIP level by decreasing its mRNA stability. Collectively, current data demonstrated that ALKBH5/CEMIP axis modulates the EMT process in NSCLC, which in turn regulates chemo-sensitivity of cancer cells to PTX.

2024-03-12 | GSE243199 | GEO

Genome binding/occupancy profiling of ALKBH5 by high throughput sequencing [Cut&Tag]

Project description:Alkylation repair homolog protein 5 (ALKBH5) binds to RNA and mediates RNA m6A demethylation. However, whether ALKBH5 binds to DNA is largely unknown. In this study, our CUT&Tag assay identified 12333 peaks in ALKBH5-overexpressing Hepa1-6 cells, indicating that ALKBH5 can bind to DNA.

2025-02-27 | GSE248568 | GEO

Genome binding/occupancy profiling of ALKBH5 by high throughput sequencing [CUT&RUN]

Project description:Alkylation repair homolog protein 5 (ALKBH5) binds to RNA and mediates RNA m6A demethylation. However, whether ALKBH5 binds to DNA is largely unknown. In this study, our CUT&RUN data show that ALKBH5 can bind to DNA in Hepa1-6 cells.

2025-02-27 | GSE277052 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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