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ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE185888 | GEO | 2022/04/13

REPOSITORIES: GEO

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ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC [RNA-seq]

Project description:To determine the targets underlying ALKBH5 during head and neck squamouse cell carcinoma progression, Methylated RNA immunoprecipitation (MeRIP) with an m6A specific antibody followed by RNA sequencing (MeRIP-seq) and next generation sequencing were combined to screen the potential targets haboring m6A modificatios and mRNA level alteration after ALKBH5 knockdown in a HNSCC cell line.

2022-04-13 | GSE185886 | GEO

ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC [MeRIP-seq]

2022-04-13 | GSE185885 | GEO

ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC

Project description:ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC

| PRJNA771102 | ENA

N6-methyladenosine demethylase ALKBH5 suppresses colorectal cancer progression potentially by decreasing PHF20 mRNA methylation.

Project description:BackgroundAs the most widespread mRNAs modification, N6-methyladenosine (m6 A) is dynamically and reversibly modulated by methyltransferases and demethylases. ALKBH5 is a major demethylase, and plays vital roles in the progression of cancers. However, the role and mechanisms of ALKBH5 in colorectal cancer (CRC) is unclear.ResultsHerein, we discovered that in CRC, downregulated ALKBH5 was closely related to poor prognosis of CRC patients. Functionally, our results demonstrated that knockdown of ALKBH5 enhanced the proliferation, migration and invasion of LOVO and RKO in vitro, while overexpression of ALKBH5 inhibited the functions of these cells. The results also demonstrated that knockdown of ALKBH5 promoted subcutaneous tumorigenesis of LOVO in vivo, while overexpression of ALKBH5 suppressed this ability. Mechanistically, results from joint analyses of MeRIP-seq and RNA-seq indicated that PHF20 mRNA was a key molecule that was regulated by ALKBH5-mediated m6 A modification. Further experiments indicated that ALKBH5 may inhibit stability of PHF20 mRNA by removing the m6 A modification of PHF20 mRNA 3'UTR.ConclusionsALKBH5 suppresses CRC progression by decreasing PHF20 mRNA methylation. ALKBH5-mediated m6 A modification of PHF20 mRNA can serve as a hopeful strategy for the intervention and treatment of CRC.

| S-EPMC9386323 | biostudies-literature

ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC [MeRIP-seq]

Project description:ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC [MeRIP-seq]

| PRJNA771104 | ENA

ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC [RNA-seq]

Project description:ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC [RNA-seq]

| PRJNA771103 | ENA

N6-methyladenosine binding induces a metal-centered rearrangement that activates the human RNA demethylase Alkbh5.

Project description:Alkbh5 catalyzes demethylation of the N6-methyladenosine (m6A), an epigenetic mark that controls several physiological processes including carcinogenesis and stem cell differentiation. The activity of Alkbh5 comprises two coupled reactions. The first reaction involves decarboxylation of α-ketoglutarate (αKG) and formation of a Fe4+═O species. This oxyferryl intermediate oxidizes the m6A to reestablish the canonical base. Despite coupling between the two reactions being required for the correct Alkbh5 functioning, the mechanisms linking dioxygen activation to m6A binding are not fully understood. Here, we use solution NMR to investigate the structure and dynamics of apo and holo Alkbh5. We show that binding of m6A to Alkbh5 induces a metal-centered rearrangement of αKG that increases the exposed area of the metal, making it available for binding O2 Our study reveals the molecular mechanisms underlying activation of Alkbh5, therefore opening new perspectives for the design of novel strategies to control gene expression and cancer progression.

| S-EPMC8373141 | biostudies-literature

The N6-methyladenosine demethylase ALKBH5 regulates the hypoxic HBV transcriptome.

Project description:Chronic hepatitis B is a global health problem and current treatments only suppress hepatitis B virus (HBV) infection, highlighting the need for new curative treatments. Oxygen levels influence HBV replication and we previously reported that hypoxia inducible factors (HIFs) activate the basal core promoter (BCP). Here we show that the hypoxic-dependent increase in BCP-derived transcripts is dependent on N6-methyladenosine (m6A) modifications in the 5' stem loop that regulate RNA half-life. Application of a probe-enriched long-read sequencing method to accurately map the HBV transcriptome showed an increased abundance of pre-genomic RNA under hypoxic conditions. Mapping the transcription start sites of BCP-RNAs identified a role for hypoxia to regulate pre-genomic RNA splicing that is dependent on m6A modification. Bioinformatic analysis of published single cell RNA-seq of murine liver showed an increased expression of the RNA demethylase ALKBH5 in the peri-central low oxygen region. In vitro studies with a human hepatocyte derived HepG2-NTCP cell line showed increased ALKBH5 gene expression under hypoxic conditions and a concomitant reduction in m6A-modified HBV BCP-RNA and host RNAs. Silencing the demethylase reduced the level of BCP-RNAs and host gene (CA9, NDRG1, VEGFA, BNIP3, FUT11, GAP and P4HA1) transcripts and this was mediated via reduced HIFα expression. In summary, our study highlights a previously unrecognized role for ALKBH5 in orchestrating viral and cellular transcriptional responses to low oxygen.

| S-EPMC10817175 | biostudies-literature

The N6-methyladenosine demethylase ALKBH5 regulates the hypoxic HBV transcriptome.

Project description:Chronic hepatitis B is a global health problem and current treatments only suppress hepatitis B virus (HBV) infection, highlighting the need for new curative treatments. Oxygen levels influence HBV replication and we previously reported that hypoxia inducible factors (HIFs) activate the basal core promoter to transcribe pre-genomic RNA. Application of a probe-enriched long-read sequencing method to map the HBV transcriptome showed an increased abundance of all viral RNAs under low oxygen or hypoxic conditions. Importantly, the hypoxic-associated increase in HBV transcripts was dependent on N6-methyladenosine (m6A) modifications and an m6A DRACH motif in the 5' stem loop of pre-genomic RNA defined transcript half-life under hypoxic conditions. Given the essential role of m6A modifications in the viral transcriptome we assessed the oxygen-dependent expression of RNA demethylases and bioinformatic analysis of published single cell RNA-seq of murine liver showed an increased expression of the RNA demethylase ALKBH5 in the peri-central low oxygen region. In vitro studies with a human hepatocyte derived HepG2 cell line showed increased ALKBH5 gene expression under hypoxic conditions. Silencing the demethylase reduced the levels of HBV pre-genomic RNA and host gene (CA9, NDRG1, VEGFA, BNIP3, FUT11, GAP and P4HA1) transcripts and this was mediated via reduced HIFα expression. In summary, our study highlights a previously unrecognized role for ALKBH5 in orchestrating viral and cellular transcriptional responses to low oxygen.

| S-EPMC10634982 | biostudies-literature

Promoting axon regeneration by inhibiting RNA N6-methyladenosine demethylase ALKBH5.

Project description:A key limiting factor of successful axon regeneration is the intrinsic regenerative ability in both the peripheral nervous system (PNS) and central nervous system (CNS). Previous studies have identified intrinsic regenerative ability regulators that act on gene expression in injured neurons. However, it is less known whether RNA modifications play a role in this process. Here, we systematically screened the functions of all common m6A modification-related enzymes in axon regeneration and report ALKBH5, an evolutionarily conserved RNA m6A demethylase, as a regulator of axonal regeneration in rodents. In PNS, knockdown of ALKBH5 enhanced sensory axonal regeneration, whereas overexpressing ALKBH5 impaired axonal regeneration in an m6A-dependent manner. Mechanistically, ALKBH5 increased the stability of Lpin2 mRNA and thus limited regenerative growth associated lipid metabolism in dorsal root ganglion neurons. Moreover, in CNS, knockdown of ALKBH5 enhanced the survival and axonal regeneration of retinal ganglion cells after optic nerve injury. Together, our results suggest a novel mechanism regulating axon regeneration and point ALKBH5 as a potential target for promoting axon regeneration in both PNS and CNS.

| S-EPMC10400074 | biostudies-literature

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