ReviewOncology letters2025
Advancements in research on the role of the key glycolytic enzyme hexokinase 2 in the regulation of tumor immune evasion (Review).
Review in Oncology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Nuclear hexokinase 2 couples hyperglycemia to MYC-driven glycolytic and stemness programs in bladder cancer.Cell death & disease · 2026Article
- Metabolic reprogramming networks in the gastric cancer tumor microenvironment: an integrated axis of nutrient competition, metabolic crosstalk, and immunosuppression.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor metabolic reprogramming is considered to be a critical driver of immune evasion. Hexokinase 2 (HK2), the initial rate-limiting enzyme of the glycolytic pathway, serves a central role in the regulatory network governing tumor metabolism and immune interactions. The expression and modification of HK2 are both influenced by various oncogenic factors and signal transduction pathways, enabling HK2 to mediate immune escape through glycolysis-dependent and independent mechanisms. In this context, HK2 can also interact with the downstream proteins of these oncogenic factors. Furthermore, the high glycolytic activity of tumor cells mediated by HK2 leads to the metabolic reprogramming of immune cells, inhibiting their activation and impairing their function, while releasing high levels of metabolic byproducts that contribute to the formation of immunosuppressive microenvironments. Targeting of metabolic pathways has emerged as a prominent area of research in counteracting immunosuppression. Due to its pivotal role in the glycolysis-driven metabolism-immune axis, HK2 has become an important target for reversing immune escape. Innovative strategies, including subcellular targeted inhibitors and combination immunotherapy, have demonstrated potential in mitigating HK2-driven immunosuppression. The present review provides a comprehensive overview of the intricate immune regulatory mechanisms that involve various signaling pathways, such as phosphatidylinositol 3-kinase/protein kinase B, mitogen-activated protein kinase, nuclear factor κ-light-chain-enhancer of activated B cells, transforming growth factor β, Janus kinase/signal transducer and activator of transcription, and HK2. The present review examines how HK2 enhances antitumor immunity by accelerating the Warburg effect and interacting with diverse immune cell subtypes, thereby contributing to the formation of an acidic, hypoxic and hypoglycemic microenvironment. Furthermore, the present review highlights the potential of HK2 as a therapeutic target and predictive biomarker.
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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 Socratic graph.