ArticleRedox biology2025
MAOB promotes ROS-mediated DNA damage, triggering a cyclic MAOB-HNF1A-53BP1-p53 axis that suppresses the malignancy of clear cell renal cell carcinoma.
Article in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- From Environmental Exposure to Intervertebral Disc Degeneration: First Evidence of Pro-Degenerative Effects of Polyamide 6 Microplastics.Biomedicines · 2026Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Monoamine oxidases (MAOA and MAOB) are mitochondrial enzymes that degrade various monoamine neurotransmitters, which have been recognized as important regulators of tumor progression. Recently, conflicting roles of both enzymes were identified in several cancer types. However, their potential involvement in the progression of clear cell renal cell carcinoma (ccRCC) remains unclear. In this study, in silico analysis of the TCGA-KIRC dataset revealed that MAOB has a more significant prognostic impact than MAOA and serves as an independent prognostic factor for overall survival in ccRCC. Lower MAOB transcript and protein levels were observed in RCC tissues compared to normal tissues and were associated with larger tumor sizes. Enzymatically active MAOB promoted reactive oxygen species (ROS)-induced DNA damage, subsequently enhancing the stability and transcriptional activity of p53, which induced G1 cell cycle arrest, mitochondria apoptosis, and lipid peroxidation-triggered ferroptosis, ultimately suppressing tumor growth both in vitro and in vivo. Molecular studies showed that MAOB stabilizes and activates p53 through post-translational modifications (PTMs), including increased phosphorylation at Ser15 and acetylation at Lys382, as well as activation of the hepatocyte nuclear factor 1 homeobox A (HNF1A)-p53-binding protein 1 (53BP1) axis. Activated p53, in turn, regulated MAOB through positive feedback. Clinically, ccRCC samples revealed a positive correlation between MAOB and HNF1A expression, with patients expressing high levels of both having the best prognoses. Regarding therapeutic aspects, we discovered that DNA methyltransferase inhibitors serve as potential MAOB inducer in ccRCC. The current findings reveal novel mechanisms by which MAOB suppresses the malignancy of ccRCC and suggest that MAOB may serve as a valuable prognostic marker in the management of ccRCC.
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.