ArticleMolecular biology of the cell2019
Tristetraprolin-mediated hexokinase 2 expression regulation contributes to glycolysis in cancer cells.
Article in Molecular biology of the cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 32 citations in OpenAlex.
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- Deletion of smooth muscle ZFP36 promotes neointimal hyperplasia in mice.Acta pharmacologica Sinica · 2025Article
- Lactate metabolism and lactylation in breast cancer: mechanisms and implications.Cancer metastasis reviews · 2025Review
- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- RHOF promotes Snail1 lactylation by enhancing PKM2-mediated glycolysis to induce pancreatic cancer cell endothelial-mesenchymal transition.Cancer & metabolism · 2024Article
- Metformin induces ZFP36 by mTORC1 inhibition in cervical cancer-derived cell lines.BMC cancer · 2024Article
- Post-translational protein lactylation modification in health and diseases: a double-edged sword.Journal of translational medicine · 2024Review
- Multiomics analysis couples mRNA turnover and translational control of glutamine metabolism to the differentiation of the activated CD4Scientific reports · 2022Article
- Moonlighting Proteins: The Case of the Hexokinases.Frontiers in molecular biosciences · 2021Review
- Tristetraprolin, a Potential Safeguard Against Carcinoma: Role in the Tumor Microenvironment.Frontiers in oncology · 2021Review
- Roquin1 inhibits the proliferation of breast cancer cells by inducing G1/S cell cycle arrest via selectively destabilizing the mRNAs of cell cycle-promoting genes.Journal of experimental & clinical cancer research : CR · 2020Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
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Abstract
Hexokinase 2 (HK2) catalyzes the first step of glycolysis and is up-regulated in cancer cells. The mechanism has not been fully elucidated. Tristetraprolin (TTP) is an AU-rich element (ARE)-binding protein that inhibits the expression of ARE-containing genes by enhancing mRNA degradation. TTP expression is down-regulated in cancer cells. We demonstrated that TTP is critical for down-regulation of HK2 expression in cancer cells. HK2 mRNA contains an ARE within its 3'-UTR. TTP binds to HK2 3'-UTR and enhances degradation of HK2 mRNA. TTP overexpression decreased HK2 expression and suppressed the glycolytic capacity of cancer cells, measured as glucose uptake and production of glucose-6-phosphate, pyruvate, and lactate. TTP overexpression reduced both the extracellular acidification rate (ECAR) and the oxygen consumption rate (OCR) of cancer cells. Ectopic expression of HK2 in cancer cells attenuated the reduction in glycolytic capacity, ECAR, and OCR from TTP. Taken together, these findings suggest that TTP acts as a negative regulator of HK2 expression and glucose metabolism in cancer cells.
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