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AMT inhibits the progression of non-small cell lung cancer by suppressing the PI3K/AKT/GSK-3β/β-catenin pathway via H3K27me3 regulation.

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European journal of pharmacology 2026 Vol.1011() p. 178460
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Gao Y, E G, Feng L, Gan P, Huang S, Tang Z, Liang Q, Wang Y, Gao Y, Zhang E

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Reprogramming of glycine metabolism is closely associated with cancer initiation and progression.

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APA Gao Y, E G, et al. (2026). AMT inhibits the progression of non-small cell lung cancer by suppressing the PI3K/AKT/GSK-3β/β-catenin pathway via H3K27me3 regulation.. European journal of pharmacology, 1011, 178460. https://doi.org/10.1016/j.ejphar.2025.178460
MLA Gao Y, et al.. "AMT inhibits the progression of non-small cell lung cancer by suppressing the PI3K/AKT/GSK-3β/β-catenin pathway via H3K27me3 regulation.." European journal of pharmacology, vol. 1011, 2026, pp. 178460.
PMID 41354296

Abstract

Reprogramming of glycine metabolism is closely associated with cancer initiation and progression. The mRNA and protein expression of aminomethyltransferase (AMT), an enzyme of the glycine cleavage system, is decreased in human non-small cell lung cancer (NSCLC) and is associated with poor prognosis. AMT overexpression significantly impaired the proliferation, migration and drug resistance of NSCLC cells. Further results demonstrated that the upregulation of AMT inhibits NSCLC progression in vivo. Moreover, the suppressive effect of AMT on NSCLC cells occurred through the downregulation of PI3K/AKT/GSK-3β/β-catenin signaling. And AMT overexpression reduces the expression of PI3K and AKT1 by increasing the level of H3K27me3. This work reveals that the negative role of AMT in regulating NSCLC progression, which emerges potential therapeutic implications.

MeSH Terms

Humans; Carcinoma, Non-Small-Cell Lung; Lung Neoplasms; Glycogen Synthase Kinase 3 beta; Proto-Oncogene Proteins c-akt; beta Catenin; Phosphatidylinositol 3-Kinases; Disease Progression; Animals; Signal Transduction; Histones; Cell Proliferation; Cell Line, Tumor; Mice; Cell Movement; Gene Expression Regulation, Neoplastic

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