M6A-modified CBX1 regulates NPC progression.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA826827 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18752900_1.fastq.gz | Fastqsanger.gz | |||
| SRR18752900_2.fastq.gz | Fastqsanger.gz | |||
| SRR18752970_1.fastq.gz | Fastqsanger.gz | |||
| SRR18752970_2.fastq.gz | Fastqsanger.gz | |||
| SRR18752971_1.fastq.gz | Fastqsanger.gz |
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Project description:Nasopharyngeal carcinoma (NPC), which arises from the nasopharyngeal pharynx, is a metastasis-prone malignancy highly prevalent in East and Southeast Asia, especially southern China. Despite progress in chemo-radiotherapeutic strategies, about 20% of NPC patients still suffer from distant metastasis, thus developing new therapeutic strategies for NPC is of vital importance. N6-methyladenosine (m6A) RNA modification, the most abundant epitranscriptomic modification in eukaryotic mRNA, has attracted great attention in cancer research because of its vital biological functions. However, little is known about the underlying molecular mechanisms between m6A modification and NPC progression. We aimed to identified differential m6A peaks by analyzing the m6A modification profile in NPC with paired tissues with or without metastasis using m6A-seq. For RNA-seq and ChIP-seq, we aimed to identified the downstream targets of CBX1 in NPC.
2023-01-04 | GSE200792 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-01-04 | GSE200794 | GEO
Project description:Both N6-methyladenosine (m6A) mediates RNA fates and ubiquitin mediates protein fates play an important role in either physiology or pathology including cancer, yet how long noncoding RNAs (lncRNAs) are involved in a link of molecular fate between m6A and ubiquitin remains unknown. Here, we reveal a role for a lncRNA Downregulated RNA in Cancer (DRAIC) to suppress tumor growth and metastasis in clear cell Renal Carcinoma (ccRCC). Mechanistically, DRAIC physically interacts with heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) and enhances its protein stability by blocking E3 ligase F-box protein 11 (FBXO11)-mediated ubiquitin and proteasome-dependent degradation. Subsequently, hnRNPA2B1 destabilizes m6A modified-type 1 insulin-like growth factor receptor (IGF1R) to lead to inhibition of ccRCC progression. Moreover, four m6A modification sites of IGF1R are identified and results in its mRNA degradation. Collectively, our findings reveal that DRAIC/hnRNPA2B1 axis regulates IGF1R mRNA expression in an m6A-dependent manner and highlights an important mechanism of IGF1R fate. These findings shed light on DRAIC/hnRNPA2B1/FBXO11/IGF1R axis as potential therapeutic targets in ccRCC and build a link of molecular fate between m6A-modified RNA and ubiquitin-modified protein.
2024-01-07 | GSE244892 | GEO
Project description:Both N6-methyladenosine (m6A) mediates RNA fates and ubiquitin mediates protein fates play an important role in either physiology or pathology including cancer, yet how long noncoding RNAs (lncRNAs) are involved in a link of molecular fate between m6A and ubiquitin remains unknown. Here, we reveal a role for a lncRNA Downregulated RNA in Cancer (DRAIC) to suppress tumor growth and metastasis in clear cell Renal Carcinoma (ccRCC). Mechanistically, DRAIC physically interacts with heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) and enhances its protein stability by blocking E3 ligase F-box protein 11 (FBXO11)-mediated ubiquitin and proteasome-dependent degradation. Subsequently, hnRNPA2B1 destabilizes m6A modified-type 1 insulin-like growth factor receptor (IGF1R) to lead to inhibition of ccRCC progression. Moreover, four m6A modification sites of IGF1R are identified and results in its mRNA degradation. Collectively, our findings reveal that DRAIC/hnRNPA2B1 axis regulates IGF1R mRNA expression in an m6A-dependent manner and highlights an important mechanism of IGF1R fate. These findings shed light on DRAIC/hnRNPA2B1/FBXO11/IGF1R axis as potential therapeutic targets in ccRCC and build a link of molecular fate between m6A-modified RNA and ubiquitin-modified protein.
2024-04-26 | GSE262500 | GEO
Project description:Both N6-methyladenosine (m6A) mediates RNA fates and ubiquitin mediates protein fates play an important role in either physiology or pathology including cancer, yet how long noncoding RNAs (lncRNAs) are involved in a link of molecular fate between m6A and ubiquitin remains unknown. Here, we reveal a role for a lncRNA Downregulated RNA in Cancer (DRAIC) to suppress tumor growth and metastasis in clear cell Renal Carcinoma (ccRCC). Mechanistically, DRAIC physically interacts with heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) and enhances its protein stability by blocking E3 ligase F-box protein 11 (FBXO11)-mediated ubiquitin and proteasome-dependent degradation. Subsequently, hnRNPA2B1 destabilizes m6A modified-type 1 insulin-like growth factor receptor (IGF1R) to lead to inhibition of ccRCC progression. Moreover, four m6A modification sites of IGF1R are identified and results in its mRNA degradation. Collectively, our findings reveal that DRAIC/hnRNPA2B1 axis regulates IGF1R mRNA expression in an m6A-dependent manner and highlights an important mechanism of IGF1R fate. These findings shed light on DRAIC/hnRNPA2B1/FBXO11/IGF1R axis as potential therapeutic targets in ccRCC and build a link of molecular fate between m6A-modified RNA and ubiquitin-modified protein.
2024-01-07 | GSE244891 | GEO
Project description:DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression [m6A-seq]
| PRJNA1025309 | ENA
Project description:Nasopharyngeal carcinoma (NPC), which arises from the nasopharyngeal pharynx, is a metastasis-prone malignancy highly prevalent in East and Southeast Asia, especially southern China. Despite progress in chemo-radiotherapeutic strategies, about 20% of NPC patients still suffer from distant metastasis, thus developing new therapeutic strategies for NPC is of vital importance. N6-methyladenosine (m6A) RNA modification, the most abundant epitranscriptomic modification in eukaryotic mRNA, has attracted great attention in cancer research because of its vital biological functions. However, little is known about the underlying molecular mechanisms between m6A modification and NPC progression. We aimed to identified differential m6A peaks by analyzing the m6A modification profile in NPC with paired tissues with or without metastasis using m6A-seq. For RNA-seq and ChIP-seq, we aimed to identified the downstream targets of CBX1 in NPC.
2023-01-04 | GSE200793 | GEO
Project description:DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression
| PRJNA1092059 | ENA
Project description:DEAD-box RNA-binding proteins (RBPs) play a significant role in RNA metabolism to achieve cellular homeostasis, including miRNA biogenesis and transcription. Hypoxia induces stemness cell-like characteristics in cancer cells and promotes malignant progression. Despite the fact that hypoxia can induce the changes in protein and RNA modification, thereby regulating downstream gene expressions, how modifications at different molecular layers interplay with each other are poorly understood. Here we show that hypoxia induces HectH9-mediated K63-linked polyubiquitination of the DEAD-box protein DDX17 as well as reduces N6-methyladenosine (m6A) marks in pri-miRNAs. While m6A potentiates DDX17 binding to pri-miRNAs, decreased m6A modifications of pri-miRNAs and increased polyubiquitination of DDX17 under hypoxia lead to decreased DDX17 binding to pri-miRNAs binding. These events enhance the association of DDX17 with the ubiquitin receptor p300 and lead to a decrease in miRNA biogenesis, especially for miRNAs regulating stemness and stemness-related genes. In addition, polyubiquitinated DDX17 together with p300 upregulates H3K56Ac levels on the stemness and stemness-related genes, resulting in enhancement of tumor initiating ability. Post-transcriptionally, decreased miRNA production, including those targeting stemness genes or stemness-related genes, also facilitates tumor initiation. Together, hypoxia triggers DDX17 poly-ubiquitination, which orchestrates dual mechanisms to increase tumor initiating ability and promote tumor progression.
2018-03-09 | PXD006059 | JPOST Repository
Project description:DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression [RNA-seq]
| PRJNA1025308 | ENA