ReviewJournal of physiology and biochemistry2026
The multifaceted role of 3-methyladenine in cancer therapy.
Review in Journal of physiology and biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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9 authors.
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Abstract
3-Methyladenine (3-MA), an early autophagy inhibitor, blocks autophagosome formation mainly by inhibiting class III phosphatidylinositol 3-kinase (PI3K) vacuolar protein sorting 34, while its concurrent inhibition of class I PI3K can produce opposing effects on autophagic flux depending on nutrient status. This Review examines the context-dependent roles of 3-MA across cancer types. When autophagy serves a pro-survival function, 3-MA-mediated inhibition tends to attenuate this protective response, thereby potentiating the cytotoxicity of chemotherapeutics, targeted drugs, and natural compounds, and helping to overcome acquired resistance. However, in some settings-such as colorectal cancer without therapeutic pressure-autophagy suppression may instead promote epithelial-mesenchymal transition and metastasis. The pharmacokinetic shortcomings and off-target effects of 3-MA have motivated the design of nanocarriers for tumor-specific co-delivery, aiming to improve bioavailability and avoid paradoxical autophagy induction. Ultimately, the lasting contribution of 3-MA may be its utility as a mechanistic probe that uncovers key autophagy regulatory nodes, paving the way for next-generation selective modulators and biomarker-driven strategies.
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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 OpenQuestion graph.