ArticleCancer cell international2020
TET2 suppresses nasopharyngeal carcinoma progression by inhibiting glycolysis metabolism.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 56 citations in OpenAlex.
- Review
- S100A2 upregulates GLUT1 expression to promote glycolysis in the progression of nasopharyngeal carcinoma.Histology and histopathology · 2024Article
- TET2 regulates early and late transitions in exhausted CD8Science advances · 2024Article
- D-mannose alleviates chronic periodontitis in rats by regulating the functions of neutrophils.BMC oral health · 2024Article
- Epigenetics and environmental health.Frontiers of medicine · 2024Review
- TET2 Is Downregulated in Early Esophageal Squamous Cell Carcinoma and Promotes Esophageal Squamous Cell Malignant Behaviors.Digestive diseases and sciences · 2024Article
- Circular RNA COL1A1 promotes Warburg effect and tumor growth in nasopharyngeal carcinoma.Discover oncology · 2024Article
- Hypoxia-induced P4HA1 overexpression promotes post-ischemic angiogenesis by enhancing endothelial glycolysis through downregulating FBP1.Journal of translational medicine · 2024Article
- Metabolic reprogramming in the pathogenesis and progression of nasopharyngeal carcinoma: molecular mechanisms and therapeutic implications.American journal of cancer research · 2024Review
- Organic Acids Derived from Saliva-amalgamated Betel Quid Filtrate Are Predicted as a Ten-eleven Translocation-2 Inhibitor.Journal of cancer prevention · 2023Article
- RhoC in association with TET2/WDR5 regulates cancer stem cells by epigenetically modifying the expression of pluripotency genes.Cellular and molecular life sciences : CMLS · 2022Article
- Engrailed homeobox 1 transcriptional regulation of COL22A1 inhibits nasopharyngeal carcinoma cell senescence through the G1/S phase arrest.Journal of cellular and molecular medicine · 2022Article
- Ascorbic acid induced TET2 enzyme activation enhances cancer immunotherapy efficacy in renal cell carcinoma.International journal of biological sciences · 2022Article
- The IRF2/CENP-N/AKT signaling axis promotes proliferation, cell cycling and apoptosis resistance in nasopharyngeal carcinoma cells by increasing aerobic glycolysis.Journal of experimental & clinical cancer research : CR · 2021Article
- The clinical prognostic value of PD-L1 after concurrent chemoradiotherapy in Chinese nasopharyngeal carcinoma patients.Annals of translational medicine · 2021Article
- TET-dependent GDF7 hypomethylation impairs aqueous humor outflow and serves as a potential therapeutic target in glaucoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Metabolic Reprogramming and Immune Evasion in Nasopharyngeal Carcinoma.Frontiers in immunology · 2021Review
- BTG1 inhibits malignancy as a novel prognosis signature in endometrial carcinoma.Cancer cell international · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNasopharyngeal carcinoma (NPC) is a common malignant tumor. Ten-eleven translocation (TET) protein 2 (TET2), an evolutionarily conserved dioxygenases, is reported to be involved in various malignant tumor developments. Here, we aim to investigate the effect of TET2 on NPC progress in vitro and in vivo, and its detailed underlying mechanism.
methodsReal-time PCR and western blotting were used to determine the expression levels of TET1/2/3 in NPC cell lines. The effects of TET2 on NPC progression were evaluated using CCK8 and invasion assays in vitro. Proteins interacted with TET2 in NPC cells were detected by immunoprecipitation and mass spectrometry. The effects of TET2 or pyruvate kinase, muscle (PKM) on glycolysis in NPC cells were examined by detecting glucose uptake and lactate production. The effects of TET2 on NPC progression were evaluated using xenograft tumor model in vivo.
resultsTET2 expression was decreased in NPC cells, and TET2 overexpression inhibited proliferation and invasion of NPC cells, which is independent on TET2's catalytic activity. In mechanism, TET2 N-terminal domain interacts with PKM in cytoplasm to prevent PKM dimers from translocating into nucleus, suppressing glycolysis in NPC cells, thereby inhibiting proliferation and invasion of NPC cells. Moreover, using xenograft tumor model, we found that TET2 knockout promoted NPC progression and decreased survival rate. However, administration with the inhibitor of PKM, shikonin, decreased the tumor volume of TET2-cas9 group, and increased the survival rate.
conclusionTET2 suppresses NPC development through interacting with PKM to inhibit glycolysis.
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