ArticleHereditas2026
NSUN2 restrains gastric cancer cell apoptosis and ferroptosis by promoting the m5C modification of EPYC.
Article in Hereditas, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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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Who cites it
1 citing paper in PubMed.
- mBiology direct · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpiphycan (EPYC) has been confirmed to play an oncogenic role in many cancers. However, its role and mechanism in gastric cancer (GC) progression has not been explored.
methodsThe levels of EPYC and NOP2/Sun domain 2 (NSUN2) were detected by qRT-PCR and western blot. Cell proliferation, apoptosis, migration and invasion were determined by cell counting kit 8 assay, colony formation assay, flow cytometry, wound healing assay and transwell assay. Fe
resultsEPYC was abnormally higher expressed in GC tissues and cells. Knockdown of EPYC restrained GC cell proliferation, migration and invasion, while enhanced apoptosis and ferroptosis. NSUN2 had elevated expression in GC, which could increase the mRNA stability and expression of EPYC through m5C modification. NSUN2 silencing inhibited GC cell proliferation, metastasis, promoted apoptosis and ferroptosis, while these effects were reversed by EPYC overexpression. In vivo experiments revealed that NSUN2 downregulation reduced GC tumorigenesis by decreasing EPYC level in vivo.
conclusionNSUN2-mediated m5C modification of EPYC contributed to GC cell growth and metastasis, which provided a novel regulatory axis for understanding the pathogenesis of GC.
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