ArticleScience advances2025
BE screen reveals METTL3 S2 dephosphorylation sensitizes gastric cancer cells to oxaliplatin by interfering METTL3-eIF3H interaction.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The resistance to oxaliplatin (OXA)-based chemotherapies may lead to poor prognosis in patients with gastric cancer (GC). Emerging evidence suggests that resistance is closely associated with phosphorylation modifications. In GC cell line AGS, high-throughput base editor screen identified key phosphorylation sites associated with OXA response. Methyltransferase-like 3 (METTL3) S2 emerged as a notable negative hit. Further investigation revealed that dephosphorylation of METTL3 S2 disrupted the METTL3-eukaryotic translation initiation factor 3 subunit H (eIF3H) interaction, thereby suppressing the translation of oncogenes involved in replication stress responses, including bromine domain protein 4 (
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.