ArticleOncotarget2016
MiR-448 promotes glycolytic metabolism of gastric cancer by downregulating KDM2B.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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
25 citing papers in PubMed, 44 citations in OpenAlex.
- Histone Methylation, Energy Metabolism, and Alzheimer's Disease.Aging and disease · 2024Review
- Roles of Lysine Methylation in Glucose and Lipid Metabolism: Functions, Regulatory Mechanisms, and Therapeutic Implications.Biomolecules · 2024Review
- F-box proteins and gastric cancer: an update from functional and regulatory mechanism to therapeutic clinical prospects.International journal of medical sciences · 2024Review
- Investigations into the impact of non-coding RNA on the sensitivity of gastric cancer to radiotherapy.Frontiers in physiology · 2023Review
- Non-coding RNAs regulate mitochondrial dynamics in the development of gastric cancer.Frontiers in molecular biosciences · 2023Review
- Epi-miRNAs: Regulators of the Histone Modification Machinery in Human Cancer.Journal of oncology · 2022Review
- Prognostic value of a novel glycolysis-related gene expression signature for gastrointestinal cancer in the Asian population.Cancer cell international · 2021Article
- DLX6 Antisense RNA 1 Modulates Glucose Metabolism and Cell Growth in Gastric Cancer by Targeting microRNA-4290.Digestive diseases and sciences · 2021Article
- Expression and Gene Regulation Network of Adenosine Receptor A2B in Lung Adenocarcinoma: A Potential Diagnostic and Prognostic Biomarker.Frontiers in molecular biosciences · 2021Article
- Interaction of ncRNA and Epigenetic Modifications in Gastric Cancer: Focus on Histone Modification.Frontiers in oncology · 2021Review
- The Complex Network between MYC Oncogene and microRNAs in Gastric Cancer: An Overview.International journal of molecular sciences · 2020Review
- Therapeutic Potentials of Inhibition of Jumonji C Domain-containing Demethylases in Acute Myeloid LeukemiaTurkish journal of haematology : official journal of Turkish Society of Haematology · 2020Article
- Lysine demethylase 2 (KDM2B) regulates hippo pathway via MOB1 to promote pancreatic ductal adenocarcinoma (PDAC) progression.Journal of experimental & clinical cancer research : CR · 2020Article
- MicroRNA-448 modulates the progression of neuropathic pain by targeting sirtuin 1.Experimental and therapeutic medicine · 2019Article
- Metabolic reprogramming results in abnormal glycolysis in gastric cancer: a review.OncoTargets and therapy · 2019Review
- HPV16 E6 and E7 upregulate the histone lysine demethylase KDM2B through the c-MYC/miR-146a-5p axys.Oncogene · 2018Article
- Epigenetic modifications inClinical epigenetics · 2018Article
- The critical role of histone lysine demethylase KDM2B in cancer.American journal of translational research · 2018Review
- MiR-361-5p inhibits glycolytic metabolism, proliferation and invasion of breast cancer by targeting FGFR1 and MMP-1.Journal of experimental & clinical cancer research : CR · 2017Article
- Prognostic value of microRNAs in gastric cancer: a meta-analysis.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs are critical in various human cancers, including gastric cancer (GC). However, the mechanism underlying the GC development remains elusive. In this study, we demonstrate that miR-448 is increased in GC samples and cell lines. Overexpression of miR-448 facilitated the proliferation of GC cells by stimulating glycolysis. Mechanistically, we identified KDM2B, a reader for methylated CpGs, as the target of miR-448 that represses glycolysis and promotes oxidative phosphorylation. Overexpression of miR-448 reduced both the mRNA and protein levels of KDM2B, whereas KDM2B re-expression abrogated the miR-448-mediated glycolytic activities. Furthermore, we discovered Myc as a key target of KDM2B that controls metabolic switch in GC. Importantly, a cohort of 81 GC tissues revealed that miR-448 level closely associated with a battery of glycolytic genes, in which KDM2B showed the strongest anti-correlation coefficient. In addition, enhanced miR-448 level was significantly associated with poor clinical outcomes of GC patients. Hence, we identified a previously unappreciated mechanism by which miR-448 orchestrate epigenetic, transcriptional and metabolic networks to promote GC progression, suggesting the possibility of therapeutic intervention against cancer metabolic pathways.
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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.