ReviewCells2026
Targeting Glycolytic Plasticity to Overcome Therapy Resistance in Cancer Stem Cells: Mechanisms and Clinical Perspectives.
Review in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Cancer stem cells (CSCs) constitute a resilient tumor subpopulation responsible for multidrug resistance, metastasis, and clinical relapse. A cardinal hallmark of these cells is profound metabolic plasticity. This dynamic defense mechanism facilitates rapid shifts between glycolysis, oxidative phosphorylation (OXPHOS), and alternative nutrient catabolism, enabling CSCs to bypass microenvironmental constraints. This review delineates how glycolytic adaptation functions as a primary driver of therapy resistance within the CSC niche. We dissect the regulatory triad controlling these metabolic shifts, which includes rate-limiting enzymes, epigenetic and epitranscriptomic remodeling, and master transcription factors. Glycolytic reprogramming transcends bioenergetics by acting as a metabolic signaling node. It integrates with the epithelial-mesenchymal transition (EMT) program, autophagic pathways, and the immunosuppressive tumor microenvironment (TME) to fortify CSC survival. We appraise emerging therapeutic interventions targeting these metabolic vulnerabilities. Strategies focus on optimizing small-molecule inhibitors, nanotechnology-enabled delivery systems, and immunometabolic combination regimens. This review establishes a conceptual framework for precision interventions aimed at disrupting CSC plasticity, overcoming therapeutic resistance, and preventing tumor recurrence.
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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.