ArticleNature communications2021
EGFR/SRC/ERK-stabilized YTHDF2 promotes cholesterol dysregulation and invasive growth of glioblastoma.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 204 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
204 citing papers in PubMed, 1 synthesis or guideline pooled it, 321 citations in OpenAlex.
- mRNA markers for survival prediction in glioblastoma multiforme patients: a systematic review with bioinformatic analyses.BMC cancer · 2024Pooled it
- Molecular mechanisms and targeted therapeutic strategies for glycolytic reprogramming in osteosarcoma.Genes & diseases · 2027Review
- The role, regulatory mechanisms, and therapeutic implications of FTO in gastrointestinal cancer.Genes & diseases · 2026Review
- MiR-146b-5p/ERBB4 Axis Drives LPS-induced Acute Kidney Injury by Modulating NF-κB/p65.Biochemical genetics · 2026Article
- LAMTOR5 drives glioblastoma progression via activation of the HOXC9/YTHDF2 positive feedback loop.The Journal of biological chemistry · 2026Article
- Review
- RNA terminal uridylyl transferases are druggable vulnerabilities in AML but are dispensable for normal hematopoiesis.Science advances · 2026Article
- mNature reviews. Neuroscience · 2026Review
- NPC2 Regulates Glioblastoma Cholesterol Metabolism and Malignant Behavior via GPX4-Linked Ferroptosis.Cell biology international · 2026Article
- Interplay between the RBP SYNCRIP and RNA methylation in determining sEV miRNA-cargo and function in cell-to-cell communication.Cell death & disease · 2026Article
- Potential anti-glioma targets and mechanisms of Smilax china L. based on network pharmacological, molecular docking and experimental verification.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- PTK6 suppresses NSCLC ferroptosis by promoting m6A-YTHDF2-dependent FOXO3 mRNA degradation through phosphorylation.Molecular genetics and genomics : MGG · 2026Article
- Targeting SRC enhances differentiation and promotes multifaceted cell death mechanisms in recurrent group 3 medulloblastoma.Cell death & disease · 2026Article
- SRC as a Prognostic and Immunomodulatory Biomarker in Acute Myeloid Leukemia: A Multi-Omics Study.International journal of molecular sciences · 2026Article
- Double-edged role of N6-methyladenosine reader YTH structural domain family protein 2 in neurological disorders: Molecular mechanisms and translational prospects.World journal of experimental medicine · 2026Review
- Mechanisms and therapeutic potential of YTHDF readers: Linking epitranscriptomics to cancer.Journal of pharmaceutical analysis · 2026Review
- NNature reviews. Cancer · 2026Review
- EGFR/ZBED1 reciprocal regulation promotes stemness and tumorigenesis in glioblastoma.Neuro-oncology · 2026Article
- Liu Wei formula ameliorates EGFR-induced malignant glioma progression by regulating EGFR/PI3K/AKT pathway and T-cell antitumor immunity.Frontiers in pharmacology · 2026Article
- A novel kinase inhibitor, Regorafenib, blocks EGFR-dependent signaling to repress tumour metastasis in human triple-negative breast cancers.Frontiers in cell and developmental biology · 2026Article
144 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM) is the most common type of adult malignant brain tumor, but its molecular mechanisms are not well understood. In addition, the knowledge of the disease-associated expression and function of YTHDF2 remains very limited. Here, we show that YTHDF2 overexpression clinically correlates with poor glioma patient prognosis. EGFR that is constitutively activated in the majority of GBM causes YTHDF2 overexpression through the EGFR/SRC/ERK pathway. EGFR/SRC/ERK signaling phosphorylates YTHDF2 serine39 and threonine381, thereby stabilizes YTHDF2 protein. YTHDF2 is required for GBM cell proliferation, invasion, and tumorigenesis. YTHDF2 facilitates m
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Registered trials
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.