ArticleEBioMedicine2022
ALKBH5 regulates STAT3 activity to affect the proliferation and tumorigenicity of osteosarcoma via an m6A-YTHDF2-dependent manner.
Article in EBioMedicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Bibliometric analysis of RNA-binding proteins in osteosarcoma: unraveling research trends and hotspots.Frontiers in immunology · 2025Pooled it
- Decoding osteosarcoma pathogenesis: the pivotal influence of mEpigenetics · 2026Review
- Article
- RNA methylation in cell death: mechanisms and clinical applications.Molecular cancer · 2026Review
- Mechanisms and therapeutic potential of YTHDF readers: Linking epitranscriptomics to cancer.Journal of pharmaceutical analysis · 2026Review
- Emerging Dual Roles of ALKBH5 in Ischemia-reperfusion Injury: Mechanisms and Therapeutic Implications.Cell biochemistry and biophysics · 2026Review
- Radiotherapy combined with anti-PD-1 immunotherapy promotes ferroptosis-driven control of hepatocellular carcinoma.Genes and immunity · 2026Article
- Context-dependent functions of ALKBH5: a mechanistic framework linking cellular stress responses, immune regulation, viral infection, and therapeutic vulnerabilities.Frontiers in immunology · 2026Review
- mFrontiers in cell and developmental biology · 2026Review
- ALKBH5 demethylation modification of SE-lncRNA ZMIZ1-AS1 promotes FGFR1-mediated proliferation and invasive metastasis in osteosarcoma.Cellular and molecular life sciences : CMLS · 2025Article
- METTL3-dependent mAutophagy · 2025Article
- The mMolecular biomedicine · 2025Review
- ALKBH5-Mediated mMolecular biotechnology · 2025Article
- KPNA2 promotes osteosarcoma progression by regulating the alternative splicing of DDX3X mediated by YBX1.Oncogene · 2025Article
- NJournal of orthopaedic translation · 2025Review
- KRAS regulates IL-17 signal activity by affect the metastasis of osteosarcoma via an IL-17A-dependent manner.JBMR plus · 2025Article
- Betaine Alleviates Bisphosphonate-Related Osteonecrosis of the Jaw by Rescuing BMSCs Function in an m6A-METTL3-Dependent Manner.International journal of molecular sciences · 2025Article
- From bone marrow mesenchymal stem cells to diseases: the crucial role of mStem cell research & therapy · 2025Review
- The Impact of METTL3 on MDM2 Promotes Podocytes Injury During Diabetic Kidney Disease.Journal of cellular and molecular medicine · 2025Article
- ALKBH5 Inhibits YTHDF2-m6A-Mediated Degradation of RCN1 mRNA to Promote Keloid Formation by Activating IRE1α-XBP1-Mediated ER Stress.Journal of cosmetic dermatology · 2025Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundN6-methyladenosine (m6A) is the most common and abundant mRNA modification and it plays crucial roles in many biological processes. However, as a key RNA demethylase, alkylation repair homolog protein 5 (ALKBH5) has not been well studied in human osteosarcoma. The present study sought to explore ALKBH5-mediated m6A modification and the underlying mechanisms in human osteosarcoma.
methodsThe expression of ALKBH5 and its correlation with clinicopathological features were examined by bioinformatics analysis and tissue microarrays. Cellular proliferation was detected by CCK8 assays. Cell cycle and apoptosis were analyzed by TUNEL and Flow cytometry assay. Finally, investigation of the regulatory mechanism of ALKBH5 in human osteosarcoma was performed by MeRIP assay, RNA-sequencing, dual luciferase reporter assay, RNA pull-down and RNA stability assay. Tumor xenograft models were established for in vivo experiments.
findingsOur data showed that low expression of ALKBH5 was associated with worse overall survival for osteosarcoma patients. Reducing m6A mRNA levels in human osteosarcoma cells through ALKBH5 up-regulation lead to cell proliferation inhibition, cell apoptosis and cycle arrest. We identified SOCS3, a negative regulator of STAT3, as a downstream target of ALKBH5-mediated m6A modification. And the m6A modified SOCS3 mRNA was recognized by YTHDF2, which promotes the decay of SOCS3. Mechanistically, our data revealed that ALKBH5 inactivated STAT3 pathway by increasing SOCS3 expression via an m6A-YTHDF2-dependent manner.
interpretationM6A methylation is rising as a pathway affecting tumorigenicity and tumor progression. Our findings illuminate the clinical significance of ALKBH5-mediated m6A modification in human osteosarcoma and the regulatory mechanisms underlying tumor proliferation and growth, suggesting that ALKBH5 is a potential biomarker for treatment in human osteosarcoma.
fundingThis work was supported by and Science and Technology foundation of Hubei, China (Grant No.2017CFB762); the Tongji hospital foundation (Grant No.2201103013); and the National Natural Science Foudation of China (No.82002849).
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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.