ArticleJournal of cancer research and clinical oncology2023
N
Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 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
- YTHDF3 Promotes the Progression of Gastric Cancer by Activating the Wnt/β-Catenin Signaling Pathway via Targeting NEK7.Journal of gastroenterology and hepatology · 2026Article
- Mechanisms and therapeutic potential of YTHDF readers: Linking epitranscriptomics to cancer.Journal of pharmaceutical analysis · 2026Review
- The role of epigenetic modifications in cancer-associated fibroblasts.Frontiers in medicine · 2026Review
- Advancing osteosarcoma treatment: the impact of intratumoral metabolic reprogramming on immunotherapy.Frontiers in immunology · 2026Review
- Influence of RNA Modifications on Cancer Metabolism: Interplay with Hypoxia and Therapeutic Implications.Advances in experimental medicine and biology · 2026Review
- From bone marrow mesenchymal stem cells to diseases: the crucial role of mStem cell research & therapy · 2025Review
- Review of the role and potential clinical value of m6A methylation modifications in the biological process of osteosarcoma.Frontiers in genetics · 2025Review
- Transcriptional regulation and post-translational modifications in the glycolytic pathway for targeted cancer therapy.Acta pharmacologica Sinica · 2024Review
- Targeting RNA modifications with pharmacological agents: New frontiers in cancer therapy.Cancer medicine · 2024Review
- RNA modifications in cellular metabolism: implications for metabolism-targeted therapy and immunotherapy.Signal transduction and targeted therapy · 2024Review
- Recent advances of m6A methylation in skeletal system disease.Journal of translational medicine · 2024Review
- Reprogramming of glucose metabolism: Metabolic alterations in the progression of osteosarcoma.Journal of bone oncology · 2024Review
- Article
- Article
- N6-methyladenosine (m6A) modification in osteosarcoma: expression, function and interaction with noncoding RNAs - an updated review.Epigenetics · 2023Review
- Molecular mechanisms of osteosarcoma metastasis and possible treatment opportunities.Frontiers in oncology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeN
methodsThe aerobic glycolysis of osteosarcoma cells were calculated by glucose uptake, lactate production analysis, ATP analysis and metabolic flux analysis for extracellular acidification rate (ECAR). Molecular binding was identified by RIP-qPCR, RNA decay analysis.
resultsResults indicated that YTHDF3 is upregulated in the osteosarcoma tissue samples and cells, and closely correlated to the poor prognosis of osteosarcoma patients. Functionally, gain and loss-of-functional assays illustrated that YTHDF3 promoted the proliferation and aerobic glycolysis of osteosarcoma cells in vitro, and accelerated the tumor growth in vivo. Mechanistically, a m
conclusionsIn conclusion, these findings indicated that YTHDF3 functioned as an oncogene in osteosarcoma tumorigenesis through m
Indexed as
Identifiers
What OpenQuestion holds
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.