ArticleCell division2025
METTL3-mediated m6A methylation of LncRNA DUXAP8 promoted esophageal squamous cell carcinoma progression by activating the PI3K/AKT signaling pathway.
Article in Cell division, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Ubiquitination and NOncology letters · 2026Review
- METTL3 in esophageal cancer: Current insights into molecular mechanisms, subtype heterogeneity and targeted therapy prospects (Review).International journal of oncology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
backgroundTo uncover the mechanism of METTL3 and LncRNA DUXAP8 in esophageal squamous cell carcinoma (ESCC) progression.
methodsLncRNA DUXAP8 expression was assessed by qRT-PCR. Its overexpression and knockdown in ESCC cells were evaluated for effects on viability and metastasis. WB analyzed PI3K/AKT signaling proteins. MeRIP and RIP assays explored METTL3-DUXAP8 interaction and m6A methylation. In vivo experiments validated the mechanism.
resultsDUXAP8 was upregulated in ESCC and enhanced cell proliferation, metastasis, and PI3K/AKT activation. It was confirmed that METTL3-DUXAP8 interaction and METTL3 mediated the m6A methylation of DUXAP8. The total level of DUXAP8 and its m6A methylation in TE-1 and KSYE-150 cell lines was decreased significantly by METTL3 knockdown, which inactivated the PI3K/AKT pathway and reduced cell proliferation and metastasis. Xenograft tumor mouse model confirmed that si-METTL3 can reverse DUXAP8-mediated ESCC proliferation via activating the PI3K/AKT pathway.
conclusionMETTL3 drives ESCC oncogenesis by binding and positively regulating DUXAP8 in an m6A-dependent manner and activating the PI3K/AKT pathway.
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