Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1255838 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33323460_1.fastq.gz | Fastqsanger.gz | |||
| SRR33323460_2.fastq.gz | Fastqsanger.gz | |||
| SRR33323461_1.fastq.gz | Fastqsanger.gz | |||
| SRR33323461_2.fastq.gz | Fastqsanger.gz | |||
| SRR33323462_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 72 |
Similar Datasets
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
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
Project description:N6-methyladenosine (m6A) modification is the most prevalent RNA epigenetic regulation in eukaryotic cells. Recent studies focused on the association between m6A and non-coding RNAs. The demethylase ALKBH5 acts as critical oncogenes or tumor suppressors through multiple mechanisms in various cancers. Here, we find that ALKBH5 is highly expressed in GC tissues and is associated with poor prognosis. ALKBH5 promoted the proliferation and metastasis both in vitro and in vivo. ALKBH5 was recruited by LINC00659, which removed m6A modifications of JAK1, leading to the upregulated expression of JAK1.Since ALKBH5 and LINC00659 have oncogenic role in gastric cancer (GC) progression with poor prognosis, ALKBH5-LINC00659/m6A/JAK1 axis can be new biological mechanisms behind GC development and future therapeutic opportunities.
2024-08-17 | GSE182544 | GEO
Project description:N6-methyladenosine (m6A) modification is the most prevalent RNA epigenetic regulation in eukaryotic cells. Recent studies focused on the association between m6A and non-coding RNAs. The demethylase ALKBH5 acts as critical oncogenes or tumor suppressors through multiple mechanisms in various cancers. Here, we find that ALKBH5 is highly expressed in GC tissues and is associated with poor prognosis. ALKBH5 promoted the proliferation and metastasis both in vitro and in vivo. ALKBH5 was recruited by LINC00659, which removed m6A modifications of JAK1, leading to the upregulated expression of JAK1.Since ALKBH5 and LINC00659 have oncogenic role in gastric cancer (GC) progression with poor prognosis, ALKBH5-LINC00659/m6A/JAK1 axis can be new biological mechanisms behind GC development and future therapeutic opportunities.
2024-08-17 | GSE182543 | GEO
Project description:N6-methyladenosine (m6A) modification is the most prevalent RNA epigenetic regulation in eukaryotic cells. Recent studies focused on the association between m6A and non-coding RNAs. The demethylase ALKBH5 acts as critical oncogenes or tumor suppressors through multiple mechanisms in various cancers. Here, we find that ALKBH5 is highly expressed in GC tissues and is associated with poor prognosis. ALKBH5 promoted the proliferation and metastasis both in vitro and in vivo. ALKBH5 was recruited by LINC00659, which removed m6A modifications of JAK1, leading to the upregulated expression of JAK1.Since ALKBH5 and LINC00659 have oncogenic role in gastric cancer (GC) progression with poor prognosis, ALKBH5-LINC00659/m6A/JAK1 axis can be new biological mechanisms behind GC development and future therapeutic opportunities.
2024-08-17 | GSE182542 | GEO
Project description:The dynamic and reversible N6-methyladenosine (m6A) RNA modification installed and erased by N6-methyltransferases and demethylases regulates gene expression and cell fate. Here, we show that the m6A demethylase ALKBH5 is highly expressed in glioblastoma stem-like cells (GSCs). Silencing ALKBH5 suppresses the proliferation of patient-derived GSCs in vitro and in vivo. Integrated transcriptome and m6A-seq analyses revealed altered expression of select ALKBH5 target genes, including FOXM1, a critical transcription factor for the ALKBH5-dependent cell cycle gene expression. ALKBH5 binds to and demethylates FOXM1 nascent transcripts, leading to enhanced FOXM1 expression. Further, a long noncoding RNA antisense to the FOXM1 (FOXM1-AS) interacts with ALKBH5 and FOXM1 nascent transcripts and promotes their interaction. Depleting ALKBH5 and FOXM1-AS disrupted GSC tumorigenesis through the FOXM1 axis. Our work uncovers a novel function for ALKBH5 in maintaining GSC tumorigenicity and provides insight into critical roles of the m6A RNA methylation in human brain tumor.
2017-03-28 | GSE87515 | GEO
Project description:N6-methyladenosine (m6A) modification is implicated in the tumorigenicity of hepatocellular carcinoma (HCC). AlkB homolog 5 (ALKBH5) is one of the m6A demethylases, and it has not been well characterized in HCC. In our study we clarify the biological roles and potential mechanisms of ALKBH5 in HCC. We identify the expression profile of ALKBH5 in HCC and find that it serves as an independent prognostic factor of HCC survival. It impacts the proliferation and invasion capability of HCC cells in vitro and in vivo. ALKBH5-mediated m6A demethylation leads to a post-transcriptional modulation of LYPD1. In addition, we reveal the tumor-related behaviors of LYPD1.
2020-08-11 | GSE149510 | GEO
Project description:Ovarian cancer (OC) is the most lethal disease among female reproductive system tumors, particularly epithelial ovarian cancer (EOC). N6-methyladenosine (m6A) is the most abundant internal modification in eukaryotic RNA and is involved in gene expression regulation. In OC, high expression of the m6A reader protein IGF2BP3 predicts a poor prognosis, but the target molecules and mechanisms underlying this association remain unclear. This study demonstrates that IGF2BP3 promotes EOC progression by recognizing and stabilizing m6A-modified FASN mRNA, thereby activating the WNT/β-catenin signaling pathway. This activation enhances lipid synthesis, increases mitochondrial membrane potential, shortens S-phase duration, and promotes cell proliferation and metastasis. Mechanistically, IGF2BP3 binds to m6A-modified FASN mRNA to enhance its stability, and pharmacological inhibition of FASN by orlistat reverses IGF2BP3-mediated oncogenic effects and WNT/β-catenin activation. In vivo and in vitro experiments confirm that knocking down either IGF2BP3 or FASN reverses these malignant phenotypes. These findings highlight a novel m6A-dependent IGF2BP3–FASN–WNT axis that drives EOC progression, providing a potential biomarker for targeted therapy.
2026-06-20 | GSE331545 | GEO
Project description:The role of N6-methyladenosine (m6A) in pancreatic ductal adenocarcinoma (PDAC) progression has garnered significant attention, yet its specific function within cancer-associated fibroblasts (CAFs)—key players in the tumor microenvironment—remains poorly understood. Here, using both primary and immortalized CAFs that we established from patient-derived samples, we identified m6A demethylase AlkB homolog 5 (ALKBH5) as a critical regulator of CAF-driven PDAC metastasis. We show that CAF activation induces a global reduction in m6A levels, with ALKBH5 emerging as a core modulator of the m6A epitranscriptome. Mechanistically, ALKBH5 enhances the m6A-dependent translational efficiency of heat shock factor 1 (HSF1), which in turn activates leukemia inhibitory factor (LIF) transcription by binding to its enhancer elements. Paracrine LIF signaling promotes epithelial–mesenchymal transition in pancreatic cancer cells, thereby facilitating tumor metastasis to the liver and lungs. Clinically, enrichment of ALKBH5+HSF1+ CAFs is strongly associated with poor prognosis and is predominantly observed in primary PDAC with metastasis. Together, this work demonstrates a CAF–intrinsic ALKBH5–HSF1–LIF axis as a critical driver of PDAC metastasis, suggesting a promising therapeutic strategy targeting the tumor stroma.
2026-06-26 | GSE304436 | GEO
Project description:The role of N6-methyladenosine (m6A) in pancreatic ductal adenocarcinoma (PDAC) progression has garnered significant attention, yet its specific function within cancer-associated fibroblasts (CAFs)—key players in the tumor microenvironment—remains poorly understood. Here, using both primary and immortalized CAFs that we established from patient-derived samples, we identified m6A demethylase AlkB homolog 5 (ALKBH5) as a critical regulator of CAF-driven PDAC metastasis. We show that CAF activation induces a global reduction in m6A levels, with ALKBH5 emerging as a core modulator of the m6A epitranscriptome. Mechanistically, ALKBH5 enhances the m6A-dependent translational efficiency of heat shock factor 1 (HSF1), which in turn activates leukemia inhibitory factor (LIF) transcription by binding to its enhancer elements. Paracrine LIF signaling promotes epithelial–mesenchymal transition in pancreatic cancer cells, thereby facilitating tumor metastasis to the liver and lungs. Clinically, enrichment of ALKBH5+HSF1+ CAFs is strongly associated with poor prognosis and is predominantly observed in primary PDAC with metastasis. Together, this work demonstrates a CAF–intrinsic ALKBH5–HSF1–LIF axis as a critical driver of PDAC metastasis, suggesting a promising therapeutic strategy targeting the tumor stroma.
2026-06-26 | GSE304433 | GEO