ArticleEpigenomics2026
ALKBH5-mediated m6A demethylation of TXNDC5 drives malignant progression in gastric cancer.
Article in Epigenomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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1 citing paper in PubMed.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGastric cancer (GC) remains a leading cause of cancer-related mortality worldwide. N6-methyladenosine (m6A) modification plays a critical role in post-transcriptional gene regulation. This study aimed to elucidate the molecular mechanism by which the RNA demethylase ALKBH5 regulates GC progression through m6A modification of thioredoxin domain-containing protein 5 (TXNDC5).
methodsDifferential expression models of ALKBH5 and TXNDC5 were established in GC cells using RNA interference and gene overexpression. Methylated RNA immunoprecipitation (MeRIP-qPCR), qPCR, and Western blot were performed to assess ALKBH5-mediated m6A modification and its effect on TXNDC5 expression. Functional assays, including proliferation, migration, and invasion, as well as a xenograft mouse model, were used to evaluate their roles in GC progression.
resultsALKBH5 was significantly upregulated in GC tissues and cells. Overexpression of ALKBH5 stabilized TXNDC5 expression in an m6A-dependent manner, thereby promoting malignant phenotypes. Conversely, ALKBH5 knockdown increased m6A methylation of TXNDC5, reduced TXNDC5 protein expression, and suppressed GC cell proliferation, migration, and invasion. In vivo experiments confirmed that loss of ALKBH5 impaired tumor growth.
conclusionsOur findings demonstrate that the ALKBH5-TXNDC5 axis drives GC progression through m6A-dependent regulation, highlighting ALKBH5 as a potential therapeutic target for GC.
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