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DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression [RNA-seq]

ABSTRACT: DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression [RNA-seq]

PROVIDER: PRJNA1025308 | ENA |

REPOSITORIES: ENA

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DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression

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

DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression [m6A-seq]

2024-01-07 | GSE244892 | GEO

DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression [RNA-seq]

2024-01-07 | GSE244891 | GEO

DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression

Project description:DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression

| PRJNA1092059 | ENA

DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression [m6A-seq]

Project description:DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression [m6A-seq]

| PRJNA1025309 | ENA

Nuclear HNRNPA2B1 HITS-CLIP and RNA-seq

Project description:To identify HNRNPA2B1 binding sites on endogenous nuclear RNAs, we performed HITS-CLIP for endogenous HNRNPA2B1 and RNA-seq to analyze the nuclear RNA under either METTL3 or HNRNPA2B1 depletion. Wild type MDA-MB-231 cells were subjected to the HITS-CLIP procedure on immunoprecipitated HNRNPA2B1 associated RNA obtained from the nuclear fraction (Licatalosi D, et al. 2008, Nature 456:464-U22). For RNA-seq, nuclear RNA was extracted from MDA-MB-231 or Hela cells knocked down for METTL3 or HNRNPA2B1.

2015-06-20 | E-GEOD-70061 | biostudies-arrayexpress

Gene expression analysis of VMRC-LD cells transfected with siRNA against DRAIC

Project description:DRAIC is a long non-coding RNA, that is involved in various cancer progressions. We performed gene expression microarray after DRAIC knockdown in VMRC-LCD cells to reveal the potential downstream genes.

2023-12-13 | GSE242691 | GEO

Nuclear HNRNPA2B1 HITS-CLIP and RNA-seq

2015-06-20 | GSE70061 | GEO

Next Generation Sequencing upon siRNA-mediated knockdown of DRAIC in MCF-7 cells.

Project description:The goal of this study is to examine the effect of DRAIC knockdown on the MCF-7 transcriptome.

2019-03-18 | GSE118101 | GEO

Transcription profiling of mouse ventricles of IGF1R, IGF1R-caPI3K, IGF1R-dnPI3K, caPI3K, dnPI3K transgenic female mice at 3 months of age vs. non transgenic littermate controls

Project description:IGF1 and IGF1 receptors (IGF1R) are present in the adult heart and have been shown to be essential for myocardial performance. Insulin-like growth factor 1 (IGF1) is produced in numerous tissues particularly by the liver in response to growth hormone stimulation and is an important factor in the regulation of post-natal growth and development. We have generated and characterized transgenic mice over-expressing the IGF1R. We crossed IGF1R transgenic mice with dominant negative (dn)PI3K (p110) and with constitutively active (ca)PI3K(p110) transgenic mice. Expression profiling was performed on the ventricles of IGF1R, IGF1R-caPI3K, IGF1R-dnPI3K, caPI3K, dnPI3K transgenic female mice at 3 months of age. Non-transgenic littermates were used as controls.

2007-09-29 | E-GEOD-1143 | biostudies-arrayexpress

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