ArticleMolecular genetics and genomics : MGG2026
PTK6 suppresses NSCLC ferroptosis by promoting m6A-YTHDF2-dependent FOXO3 mRNA degradation through phosphorylation.
Article in Molecular genetics and genomics : MGG, 2026. 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
7 authors.
Funding
Abstract
Ferroptosis has emerged as a potential therapeutic target for non-small cell lung cancer (NSCLC), but its regulatory mechanisms remain elusive. Protein tyrosine kinase 6 (PTK6) is overexpressed in NSCLC and linked to poor prognosis, though its role in ferroptosis is unknown. CCK-8 assay was performed to assess cell viability. Intracellular Fe2+ level was measured using an iron assay kit. Lipid peroxidation was evaluated using the C11 BODIPY probe. Dual-luciferase reporter and ChIP assays were employed to investigate FOXO3’s interaction with the APOL3 promoter. PTK6-YTHDF2 interaction was examined using Co-IP assay, and YTHDF2-FOXO3 interaction was detected using RIP assay. PTK6 knockdown exacerbated Erastin-induced ferroptosis in NSCLC cells. Mechanistically, PTK6 enhanced YTHDF2-mediated FOXO3 mRNA degradation by phosphorylating YTHDF2. FOXO3 silencing reversed PTK6 depletion’s pro-ferroptotic effects. FOXO3 transcriptionally activated APOL3 expression. APOL3 knockdown negated PTK6 silencing-driven ferroptosis sensitization. PTK6 inhibited NSCLC cells ferroptosis by promoting m6A-YTHDF2-dependent FOXO3 mRNA degradation through phosphorylating YTHDF2, thereby suppressing FOXO3-mediated APOL3 transcriptional activation.
Indexed as
Identifiers
42029771What 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.