ArticleAnimal cells and systems2019
KAT5 Negatively regulates the proliferation of prostate cancer LNCaP cells via the caspase 3-dependent apoptosis pathway.
Article in Animal cells and systems, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- KAT5 promotes tumor growth in androgen-independent prostate cancer by facilitating aerobic glycolysis.Translational oncology · 2025Article
- Lysine acetyltransferase 5 contributes to diabetic retinopathy by modulating autophagy through epigenetically regulating autophagy-related gene 7.CytoJournal · 2025Article
- Epigenetic insights into prostate cancer: exploring histone modifications and their therapeutic implications.Frontiers in oncology · 2025Review
- Review
- STUB1 is acetylated by KAT5 and alleviates myocardial ischemia-reperfusion injury through LATS2-YAP-β-catenin axis.Communications biology · 2024Article
- ZNF692 drives malignant development of hepatocellular carcinoma cells by promoting ALDOA-dependent glycolysis.Functional & integrative genomics · 2024Article
- Knockdown of KAT5/KIF11 induces autophagy and promotes apoptosis in anaplastic thyroid cancer cells.Experimental and therapeutic medicine · 2023Article
- Article
- KAT5 histone acetyltransferase mutations in cancer cells.microPublication biology · 2022Article
- Article
- Post-Translational Modifications That Drive Prostate Cancer Progression.Biomolecules · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer is one of the most common cancers in men over the age of sixty. Lysine acetyltransferase 5 (KAT5) is a histone acetyltransferase involved in transcriptional regulation, DNA repair, and cell signaling pathways. Previous studies have shown that KAT5 expression is reduced in the cytoplasm of the prostate cancer cell line LNCaP when exposed to androgen. Moreover, KAT5 has been reported to have a role in the molecular pathway leading to androgen-independent prostate cancer after long-term androgen deprivation therapy. Here, we showed that KAT5 expression was significantly reduced in prostate cancer tissues and cell lines by using the public databases Oncomine and Human Protein Atlas. Reduced KAT5 expression was significantly associated with high mortality in prostate cancer patients. Furthermore, KAT5 overexpression increased the level of apoptotic markers, such as cleaved-caspase 3, in LNCaP cells, thus enhancing the apoptotic death of LNCaP cells. Taken together, KAT5 induced apoptosis in prostate cancer cells via the caspase-3 pathway, indicating that KAT5 could be a gene therapy target for prostate 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 OpenQuestion graph.