ArticleProceedings of the National Academy of Sciences of the United States of America2024
KDM5D histone demethylase mediates p38α inactivation via its enzymatic activity to inhibit cancer progression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed.
- Article
- Beyond sex determination: the Y chromosome in male cancers.Nature reviews. Cancer · 2026Review
- [DOT1L controls neuronal amyloid precursor protein expres-sion via the p38 MAPK-mediated mitochondrial dynamics homeostasis axis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Article
- Sexual Dimorphism in Allergic and Mast Cell-Associated Diseases.Clinical reviews in allergy & immunology · 2026Review
- Targeting p38α in cancer: challenges, opportunities, and emerging strategies.Molecular oncology · 2026Review
- Article
- Histone lysine demethylases in breast cancer: molecular mechanisms, biological functions, and therapeutic intervention.Molecular cancer · 2025Review
- Lysine demethylase 5D promotes CHEK1 inhibitor sensitivity through p38-mediated cyclooxygenase-2 expression in castration-resistant prostate cancer cells.The Journal of pharmacology and experimental therapeutics · 2025Article
- Y-chromosome alteration and its impact on cancer progression and metastasis.Cellular & molecular biology letters · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The p38 MAP kinase (MAPK) signaling pathway plays pivotal roles in various cellular processes. Phosphorylation serves as a canonical way to regulate p38α activation through a phosphorylation cascade. Thus, understanding the mechanism governing p38α phosphorylation is important. The present study demonstrated that p38α undergoes methylation at K165, which promote its phosphorylation in tumor cells. Inhibition of p38α methylation impairs p38α phosphorylation, repressing tumor progression in vitro and in vivo. Mechanistically, KDM5D is a demethylase that interacts with p38α, mediating demethylation at K165 and inhibiting p38α phosphorylation. Moreover, KDM5D is expressed at low levels in non-small cell lung cancer (NSCLC), and high KDM5D expression is positively correlated with cancer survival. KDM5D markedly inhibits cell proliferation and migration via inactivating p38α, thereby slowing cancer progression in xenograft models. In summary, these findings highlight KDM5D as a demethylase of p38α at K165, elucidating a unique role for lysine demethylation in integrating cytoplasmic kinase-signaling cascades. The present results revealed the critical role of KDM5D in suppressing tumor progression, suggesting that KDM5D can serve as a potential drug target for combating hyperactive p38α-driven lung cancer.
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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 Socratic graph.