ArticleInternational journal of endocrinology2022
KAT5 Inhibitor NU9056 Suppresses Anaplastic Thyroid Carcinoma Progression through c-Myc/miR-202 Pathway.
Article in International journal of endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Tumor microenvironment-guided targeted and immunotherapy in anaplastic thyroid cancer: a literature review from preclinical models to clinical translation.Translational cancer research · 2026Review
- DNA Damage and Repair in Thyroid Physiology and Disease.Endocrine reviews · 2026Review
- miR-202-5p mitigates the advancement of osteoporosis through the regulation of PTEN.Journal of orthopaedic surgery and research · 2025Article
- Sialylated IgG-activated integrin β4-Src-Erk axis stabilizes c-Myc in a p300 lysine acetyltransferase-dependent manner to promote colorectal cancer liver metastasis.Neoplasia (New York, N.Y.) · 2025Article
- TIP60 enhances cisplatin resistance via regulating ΔNp63α acetylation in SCC.Cell death & disease · 2024Article
- Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Anaplastic thyroid carcinoma (ATC) is considered to be one of the most aggressive cancers. Our previous study proved that highly expressed lysine acetyltransferase 5 (KAT5) in ATC is associated with a poorer prognosis. Here, this study examined the effects of a KAT5 inhibitor (NU9056) in human ATC cells. Methods: First, the Results: KAT5 dysregulation correlated with more advanced-stage and poorer outcomes of thyroid carcinoma patients. Endogenous KAT5 protein and mRNA levels were much higher in ATC cells than in normal thyroid cells. Suppression of KAT5 by NU9056 inhibited survival, growth, migration, invasion, and tube formation, and increased radiosensitivity and chemosensitivity in ATC cells but showed no impact on normal thyroid cells. Mechanistically, microRNA-202-5p (miR-202) was identified as the most significantly decreased miRNA after NU9056 treatment. Knockdown of miR-202 suppressed ATC cell progression, while forced expression of miR-202 partially blocked the inhibitory effect of NU9056 on ATC cells. Furthermore, c-Myc was validated as the transcription factor of miR-202, and NU9056 decreased the c-Myc protein level by shortening its half-life. Finally, we proved that NU9056 inhibited ATC proliferation in vivo. Conclusions: Our results indicated that NU9056 targets KAT5, shortens c-Myc half-life, subsequently downregulates miR-202 expression, and results in the suppression of ATC cells. Overall, KAT5 could be a potential target for clinical treatment for ATC.
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Registered trials
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