ArticleMolecular biology reports2025
METTL3 drives malignant progression in TP53-mutant prostate cancer.
Article in Molecular biology reports, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProstate cancer patients harboring TP53 mutations exhibit a more aggressive and chemo-resistant phenotype. Unfortunately, attempts to identify the vulnerabilities that could be exploited to overcome these aggressive malignancies have made only minimal progress in recent years. Consequently, there is an immediate requirement to investigate novel therapeutic strategies for this subclass. METTL3 complex, knowing to govern m6A dynamic alteration, has been suggested to be a critical therapeutic target across human cancer. However, the role of METTL3 in prostate cancer harboring TP53 mutations is totally unknown. MATERIALS AND
methodsBioinformatic analysis was employed to assess the transcriptome signature between TP53WT and TP53Mut prostate cancer and the expression of METTL3 complex in TP53WTand TP53Mutprostate cancer. Colony formation and growth curve analyses were employed to assess the role of METTL3 in TP53Mut prostate cancer. Furthermore, the bioinformatic analyses were utilized for uncovering the underlying mechanism of how METTL3 maintained the malignancy phenotype of TP53Mut prostate cancer.
resultsTP53 as one of the most frequently mutated genes in prostate cancer. Transcriptome analysis revealed that TP53 mutation significantly downregulated genes associated with prohibiting proliferation. Moreover, the core catalytic subunit, METTL3, was found to be aberrantly upregulated in TP53 mutated prostate cancer compared to that in normal and TP53WT prostate tissues. Notably, pharmaceutically blockade of METTL3 drastically inhibited TP53 mutated prostate cancer cells growth. Bioinformatic analysis suggested that METTL3 inhibition maintained TP53 mutated prostate cancer malignancies via activating MAPK signaling.
conclusionsMETTL3 serves as a novel targetable vulnerability for prostate cancer. Targeting METTL3 prohibits the TP53 mutated prostate cancer growth by inactivating MAPK signaling.
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.