ArticleCell death & disease2024
The m6A reader HNRNPC promotes glioma progression by enhancing the stability of IRAK1 mRNA through the MAPK pathway.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- circNLK restrains glioblastoma malignancy by binding to hnRNP L and destabilizing RGS16.Non-coding RNA research · 2026Article
- HNRNPC contributes to ccRCC progression by stabilizing AURKB mRNA in an m6A-dependent manner.Human cell · 2026Article
- Long-read transcriptomic profiling of a glioma cell line following m6A regulator perturbations.Biochemistry and biophysics reports · 2026Article
- Repurposed hnRNPC binds mature mRNAs and safeguards the mitotic transcriptome.Nucleic acids research · 2026Article
- CASC19 stabilization by ALYREF via m5C modification and its impact on SCD in colorectal cancer cell aggressiveness and stemness.Cell & bioscience · 2026Article
- Positive Feedback Loop of Histone Lactylation-Driven HNRNPC Promotes Autophagy to Confer Pancreatic Ductal Adenocarcinoma Gemcitabine Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Astrocytic Mettl14 depletion enhances cognitive function by attenuating astrogliosis via the DUSP1/MAPK pathway in APP/PS1 mice: targeting neuroinflammation in Alzheimer's disease.Molecular psychiatry · 2026Article
- Integration of network toxicology and transcriptomics reveals the potential regulatory role of the 'Arecoline/4-NQO-AKT1-m6A factor' axis in the development of OSCC.Frontiers in oncology · 2026Article
- Network-Based Prediction of Oligodendroglioma Driver Gene Candidates within the Region of the 1p/19q Co-deletion Utilizing Single-Cell Transcriptomes.Computational and structural biotechnology journal · 2026Article
- RNA methylation modifications in neurodegenerative diseases: Focus on their enzyme system.Journal of advanced research · 2025Review
- Identification of a novel m6A RNA methylation regulator-based signature for prognosis and immune landscape prediction in hepatocellular carcinoma.Scientific reports · 2025Article
- mEpigenomes · 2025Review
- Deregulating m6A regulators leads to altered RNA biology in glioma cell lines.bioRxiv : the preprint server for biology · 2025Article
- N6-methyladenosine methylation: a novel key to unlocking mental disorders.The international journal of neuropsychopharmacology · 2025Review
- Epitranscriptomics Regulation of CD70, CD80, and TIGIT in Cancer Immunity.International journal of molecular sciences · 2025Article
- The HNRNPC/CELF2 signaling pathway drives glycolytic reprogramming and mitochondrial dysfunction in drug-resistant acute myeloid leukemia.Cell & bioscience · 2025Article
- Targeting PSMD14 combined with arachidonic acid induces synthetic lethality via FADS1 mScience advances · 2025Article
- Heterogeneous nuclear ribonucleoprotein C promotes non-small cell lung cancer progression by enhancing XB130 mRNA stability and translation.Cancer cell international · 2025Article
- Novel RNA-methylase HNRNPC promotes gastric cancer tumorigenesis by triggering the lactate-induced ferroptosis resistance.Frontiers in immunology · 2025Article
- The role of N(6)-methyladenosine (m6a) modification in cancer: recent advances and future directions.EXCLI journal · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
Abstract
Glioma is the most common and aggressive type of primary malignant brain tumor. The N6-methyladenosine (m6A) modification widely exists in eukaryotic cells and plays an important role in the occurrence and development of human tumors. However, the function and mechanism of heterogeneous nuclear ribonucleoprotein C (HNRNPC), an RNA-binding protein and m6A reader in gliomas remains to be comprehensively and extensively explored. Herein, we found that HNRNPC mRNA and protein overexpression were associated with a poor prognosis for patients with gliomas, based on the data from TCGA, the CGGA, and the TMAs. Biologically, HNRNPC knockdown markedly repressed malignant phenotypes of glioma in vitro and in vivo, whereas ectopic HNRNPC expression had the opposite effect. Integrative RNA sequencing and MeRIP sequencing analyses identified interleukin-1 receptor-associated kinase 1 (IRAK1) as a downstream target of HNRNPC. The glioma public datasets and tissue microarrays (TMAs) data indicated that IRAK1 overexpression was associated with poor prognosis, and IRAK1 knockdown significantly repressed malignant biological behavior in vitro. Mechanistically, HNRNPC maintains the mRNA stability of IRAK1 in an m6A-dependent manner, resulting in activation of the mitogen-activated protein kinase (MAPK) signaling pathway, which was necessary for the malignant behavior of glioma. Our findings demonstrate the HNRNPC-IRAK1-MAPK axis as a crucial carcinogenic factor for glioma and the novel underlying mechanism of IRAK1 upregulation, which provides a rationale for therapeutically targeting epitranscriptomic modulators in glioma.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.