ArticleOncogene2026
TAF1 acetyltransferase promotes colorectal carcinoma metastasis by catalyzing β-hydroxybutyrylation of KCTD9.
Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Protein modification systems as cancer biomarkers and therapeutic targets.Precision clinical medicine · 2026Review
- TAF1 Suppresses MHC-I Expression and Correlates with Poor Immunotherapy Response in Small Cell Lung Cancer.Biomedicines · 2026Article
- Review
- Claudin-1 Interacts with CD81 and Promotes the Progression of Colorectal Cancer.Oncology research · 2026Article
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Authors and funding
13 authors.
Funding
Abstract
Colorectal carcinoma (CRC) ranks as the second leading cause of cancer mortality worldwide. However, the mechanisms underlying CRC progression and metastasis, remain unclear. Our current research has identified that TATA-binding protein-associated factor-1 (TAF1), also as a lysine acetyltransferase, is frequently upregulated in CRC. Survival analysis has indicated that patients whose tumors expressed high TAF1 levels had poorer outcomes. Additionally, TAF1 overexpression fosters CRC proliferation, colorectal cancer stem-like cell stemness (CRCSC), and metastasis. Mechanistically, we first reported that lysine β-hydroxybutyrylation (Kbhb) modification of KCTD9 at K123 and K129, mediated by TAF1, facilitates the binding of TRIM21, thereby mediating the ubiquitination degradation of KCTD9. This event consequently suppresses KCTD9 protein expression to activate Notch signaling pathway, ultimately enhancing CRC progression and metastasis. Moreover, the concomitant upregulation of TAF1 and KCTD9 Kbhb serves as a poor prognostic factor for metastatic CRC patients. Taken together, our findings bridge the newly identified Kbhb modification dependent regulatory mechanism that modulates the anticancer function of KCTD9, and provided insight into potential strategies for targeting epigenetic factor and combating the KCTD9 inactive-driven CRC metastasis.
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