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ALKBH5 cooperated with LINC00659 promote gastric cancer progression by JAK1 mRNA m6A-YTHDF2-dependent modification

ABSTRACT: ALKBH5 cooperated with LINC00659 promote gastric cancer progression by JAK1 mRNA m6A-YTHDF2-dependent modification

PROVIDER: PRJNA756697 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15559555_1.fastq.gz	Fastqsanger.gz
	SRR15559555_2.fastq.gz	Fastqsanger.gz
	SRR15559556_1.fastq.gz	Fastqsanger.gz
	SRR15559556_2.fastq.gz	Fastqsanger.gz
	SRR15559557_1.fastq.gz	Fastqsanger.gz

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ALKBH5 cooperated with LINC00659 promote gastric cancer progression by JAK1 mRNA m6A-YTHDF2-dependent modification

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

ALKBH5 cooperated with LINC00659 promote gastric cancer progression by JAK1 mRNA m6A-YTHDF2-dependent modification [polyA]

2024-08-17 | GSE182543 | GEO

ALKBH5 cooperated with LINC00659 promote gastric cancer progression by JAK1 mRNA m6A-YTHDF2-dependent modification [2-m6A]

2024-08-17 | GSE182542 | GEO

ALKBH5 cooperated with LINC00659 promote gastric cancer progression by JAK1 mRNA m6A-YTHDF2-dependent modification [polyA]

Project description:ALKBH5 cooperated with LINC00659 promote gastric cancer progression by JAK1 mRNA m6A-YTHDF2-dependent modification [polyA]

| PRJNA756696 | ENA

ALKBH5 cooperated with LINC00659 promote gastric cancer progression by JAK1 mRNA m6A-YTHDF2-dependent modification [2-m6A]

Project description:ALKBH5 cooperated with LINC00659 promote gastric cancer progression by JAK1 mRNA m6A-YTHDF2-dependent modification [2-m6A]

| PRJNA756695 | ENA

LINC00659 cooperated with ALKBH5 to accelerate gastric cancer progression by stabilising JAK1 mRNA in an m<sup>6</sup> A-YTHDF2-dependent manner.

Project description:BackgroundN6-methyladenosine (m6 A) RNA modification is known as a common epigenetic regulation form in eukaryotic cells. Emerging studies show that m6 A in noncoding RNAs makes a difference, and the aberrant expression of m6 A-associated enzymes may cause diseases. The demethylase alkB homologue 5 (ALKBH5) plays diverse roles in different cancers, but its role during gastric cancer (GC) progression is not well known.MethodsThe quantitative real-time polymerase chain reaction, immunohistochemistry staining and western blotting assays were used to detect ALKBH5 expression in GC tissues and human GC cell lines. The function assays in vitro and xenograft mouse model in vivo were used to investigate the effects of ALKBH5 during GC progression. RNA sequencing, MeRIP sequencing, RNA stability and luciferase reporter assays were performed to explore the potential molecular mechanisms involved in the function of ALKBH5. RNA binding protein immunoprecipitation sequencing (RIP-seq), RIP and RNA pull-down assays were performed to examine the influence of LINC00659 on the ALKBH5-JAK1 interaction.ResultsALKBH5 was highly expressed in GC samples and associated with aggressive clinical features and poor prognosis. ALKBH5 promoted the abilities of GC cell proliferation and metastasis in vitro and in vivo. The m6 A modification on JAK1 mRNA was removed by ALKBH5, which resulted in the upregulated expression of JAK1. LINC00659 facilitated ALKBH5 binding to and upregulated JAK1 mRNA depending on an m6 A-YTHDF2 manner. Silencing of ALKBH5 or LINC00659 disrupted GC tumourigenesis via the JAK1 axis. JAK1 upregulation activated the JAK1/STAT3 pathway in GC.ConclusionALKBH5 promoted GC development via upregulated JAK1 mRNA expression mediated by LINC00659 in an m6 A-YTHDF2-dependent manner, and targeting ALKBH5 may be a promising therapeutic method for GC patients.

| S-EPMC9982078 | biostudies-literature

Essential role of ALKBH5-mediated RNA demethylation modification in bile acid-induced gastric intestinal metaplasia

Project description:Reflux of bile acids and subsequent caudal-related homeobox 2 (CDX2) activation contribute to gastric intestinal metaplasia (IM), which is a precursor of gastric cancer. However, the underlying mechanism by which bile acids cause this is not entirely clear. Here we demonstrated that alkylation repair homolog protein 5 (ALKBH5), which is a major RNA N6-adenosine demethylase, was required for bile acid-induced gastric IM. Mechanistically, we revealed the N6-methyladenosine (m6A) modification profile in gastric IM for the first time and identified ZNF333 as a bona fide m6A target of ALKBH5. ALKBH5 was shown to demethylate ZNF333 mRNA, leading to enhanced ZNF333 expression by abolishing m6A-YTHDF2-dependent mRNA degradation. In addition, ALKBH5 activated CDX2 and downstream intestinal markers by targeting the ZNF333/CYLD axis and activating NF-κB signaling. Reciprocally, p65, which is the key transcription factor of the canonical NF-κB pathway, enhanced the transcription activity of ALKBH5 in the nucleus, thus forming a positive feed-forward circuit. In addition, ALKBH5 levels were positively correlated with ZNF333 and CDX2 in IM tissues, indicating a significant clinical relevance. Collectively, our findings suggest an m6A modification-associated positive feed-forward loop between ALKBH5 and NF-κB signaling is involved in the generation of the IM phenotype from gastric epithelial cells. Targeting the ALKBH5/ZNF333/CYLD/CDX2 axis might be a useful therapeutic strategy for gastric IM in patients with bile regurgitation.

2021-10-14 | GSE179185 | GEO

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 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [CUT&Tag]

Project description:N6-methyladenonsine (m6A) modification locates ubiquitously in mammalian mRNA, and profoundly impacts various physiological processes and pathogenesis. However, the precise involvement of m6A in early endoderm development has yet to be fully elucidated. Here, we reported that depletion of the m6A demethylase ALKBH5 in human embryonic stem cells (hESCs) severely impaired definitive endoderm (DE) differentiation. Within this process, ALKBH5-/- hESCs failed to undergo the primitive streak (PS) intermediate transition, which is considered as a prelude to endoderm specification. Mechanistically, we demonstrated that ALKBH5 deficiency induced m6A hypermethylation around the 3’ untranslated region (3’UTR) of GATA6 transcripts and destabilized GATA6 mRNA in a YTHDF2-dependent manner. Moreover, dysregulation of GATA6 expression ablated its occupancy with critical regulators of Wnt/β-catenin signaling pathway, thereby disrupting the signaling logic underlying DE formation. Overall, our findings unveil a mechanism whereby the ALKBH5-GATA6-WNT/β-catenin axis modulates human in vitro DE induction, and present novel insights on m6A modification in early embryonic development.

2024-10-23 | GSE248527 | GEO