ArticleCell death and differentiation2024
HKDC1 functions as a glucose sensor and promotes metabolic adaptation and cancer growth via interaction with PHB2.
Article in Cell death and differentiation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- HKDC1 as a Prognostic and Tumor Microenvironment‑Associated Biomarker in Colorectal Cancer: An Integrated Multi‑omics and Spatial Transcriptomic Study.Digestive diseases and sciences · 2026Article
- Patient-specific modeling identifies metabolic interventions for reversing glucose use reprogramming in alcohol-associated hepatitis.Communications biology · 2026Article
- The HKDC1-ASS1-ACSBG2 axis reprograms lipid metabolism to drive therapeutic resistance in hepatocellular carcinoma.Journal of translational medicine · 2026Article
- Single-cell and multi-omics integrative modeling identifies mitochondrial gene HSPE1 as a therapeutic target in osteosarcoma.Journal of translational medicine · 2026Article
- Circadian Clock Genes in Colorectal Cancer: From Molecular Mechanisms to Chronotherapeutic Applications.Biomedicines · 2026Review
- Glucose metabolism and its direct action in cancer and immune regulation: opportunities and challenges for metabolic targeting.Journal of biomedical science · 2025Review
- Role of PHB2 as a potential biomarker in pan-cancer: a multi-database analysis.Scientific reports · 2025Article
- Deletion of epithelial HKDC1 decelerates cellular proliferation and impairs mitochondrial function of tumorous epithelial cells thereby protecting from intestinal carcinogenesis.Cancer communications (London, England) · 2025Article
- METTL3 mediated m6A modification of HKDC1 promotes renal injury and inflammation in lead nephropathy.International journal of biological sciences · 2025Article
- A novel glucose sensor fuelling cancer growth.Cell death and differentiation · 2024Article
- Role of tumor microenvironment composition and metabolism in lymphoid malignancies and therapeutic strategies.Cell transplantationReview
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Authors and funding
8 authors.
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Abstract
Glucose sensing and metabolic adaptation to glucose availability in the tumor microenvironment are critical for cancer development. Here we show that HKDC1, a hexokinase highly expressed in cancer associated with poor prognosis, functions as a glucose sensor that alters its stability in response to environmental glucose. The glucose-sensing domain is located between amino acids 751-917, with Ser896 as a key residue that regulates HKDC1 stability by affecting Lys620 ubiquitination. This sensing mechanism enables cellular adaptation to glucose starvation by promoting mitochondrial fatty acid utilization. Furthermore, HKDC1 promotes tumor growth by sequestering prohibitin 2 (PHB2) to disable its suppressive effect on SP1, thus promoting the expression of pro-oncogenic molecules. Abrogation of HKDC1 by genetic knockout or by glucose depletion releases PHB2, leading to suppression of cancer cell proliferation and inhibition of tumor growth. Our study reveals a previously unrecognized role of HKDC1 in glucose sensing and metabolic adaptation, and identifies HKDC1 as a potential therapeutic target.
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