ArticleScientific reports2020
Vitamin K2 promotes PI3K/AKT/HIF-1α-mediated glycolysis that leads to AMPK-dependent autophagic cell death in bladder cancer cells.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 66 citations in OpenAlex.
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- Nano-bionic bacteria armed adoptive macrophage therapy against bladder cancer.Materials today. Bio · 2026Article
- The anti-leukemic effects of vitamin K4 by modulating the JAK/STAT signaling pathway.Cancer cell international · 2026Article
- Intersection of Precision Nutrition and Bladder Cancer: A Narrative State-of-the-Art Review of Potential Applications and Challenges.Journal of clinical medicine · 2026Review
- Combined vitamins D3 and K2 as potential modulators of multiple myeloma cell pathophysiology: transcriptomic and epigenetic effects under standard culture and bone marrow-like conditions.Frontiers in oncology · 2026Article
- Aerobic glycolysis in bladder cancer: research advances and targeted therapy potential.Frontiers in oncology · 2026Review
- Regulation of drug resistance in bladder urothelial carcinoma by tumor aerobic glycolysis.Journal of translational medicine · 2025Review
- Evolving strategies of intracellular HypervirulentVirulence · 2025Article
- Association Between Dietary Vitamin K Intake With Cancer Cachexia and Mortality: NHANES 1999-2018.Food science & nutrition · 2025Article
- Inherited Genetic Variation in Parkinson's Disease: Convergence on Impaired Autophagosome-Lysosome Fusion Through the Altered Expression of mRNA Isoforms.Molecular neurobiology · 2025Article
- Insights into the Molecular Mechanisms of Bushen Huoxue Decoction in Breast CancerCurrent computer-aided drug design · 2025Article
- Cirsiliol suppresses malignant progression of hepatocellular carcinoma via regulation of glutamine metabolism.American journal of translational research · 2025Article
- Circ_0081343 promotes autophagy and alleviates pyroptosis via PI3 K/AKT/HIF-1α axis in hypoxia-induced fetal growth restriction of mice.Animal cells and systems · 2025Article
- The role of glycolysis in tumorigenesis: From biological aspects to therapeutic opportunities.Neoplasia (New York, N.Y.) · 2024Review
- Elevated RBP4 in Subclinical Ketosis Cows Inhibits Follicular Granulosa Cell Proliferation and Steroid Hormone Synthesis.Animals : an open access journal from MDPI · 2024Article
- Therapeutic importance and diagnostic function of circRNAs in urological cancers: from metastasis to drug resistance.Cancer metastasis reviews · 2024Review
- Vitamin K2 in Health and Disease: A Clinical Perspective.Foods (Basel, Switzerland) · 2024Review
- Protective Effect of Vitamin K2 (MK-7) on Acute Lung Injury Induced by Lipopolysaccharide in Mice.Current issues in molecular biology · 2024Article
- Inhibition of TNBC Cell Growth by Paroxetine: Induction of Apoptosis and Blockage of Autophagy Flux.Cancers · 2024Article
- The Role of Hypoxia-inducible Factor-1 in Bladder Cancer.Current molecular medicine · 2024Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vitamin K2 has been shown to exert remarkable anticancer activity. However, the detailed mechanism remains unclear. Here, our study was the first to show that Vitamin K2 significantly promoted the glycolysis in bladder cancer cells by upregulating glucose consumption and lactate production, whereas inhibited TCA cycle by reducing the amounts of Acetyl-CoA. Moreover, suppression of PI3K/AKT and HIF-1α attenuated Vitamin K2-increased glucose consumption and lactate generation, indicating that Vitamin K2 promotes PI3K/AKT and HIF-1α-mediated glycolysis in bladder cancer cells. Importantly, upon glucose limitation, Vitamin K2-upregulated glycolysis markedly induced metabolic stress, along with AMPK activation and mTORC1 pathway suppression, which subsequently triggered AMPK-dependent autophagic cell death. Intriguingly, glucose supplementation profoundly abrogated AMPK activation and rescued bladder cancer cells from Vitamin K2-triggered autophagic cell death. Furthermore, both inhibition of PI3K/AKT/HIF-1α and attenuation of glycolysis significantly blocked Vitamin K2-induced AMPK activation and subsequently prevented autophagic cell death. Collectively, these findings reveal that Vitamin K2 could induce metabolic stress and trigger AMPK-dependent autophagic cell death in bladder cancer cells by PI3K/AKT/HIF-1α-mediated glycolysis promotion.
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