ArticleCell death & disease2025
Deacetylation of TALDO1 by HDAC6 promotes glycolysis and nasopharyngeal carcinoma progression through a moonlighting function.
Article in Cell death & disease, 2025. 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.
- Histone deacetylases in cancer metabolic reprogramming.Experimental & molecular medicine · 2026Review
- Post-translational modifications in metabolic reprogramming: implications for metabolic therapy and immunotherapy in cancer.Signal transduction and targeted therapy · 2026Review
- How to Employ Trained Immunity and Trained Immunity-Based Vaccines to Inhibit Allergic Inflammation.Vaccines · 2026Review
- Role of HDAC6 in carcinomas.Discover oncology · 2026Review
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Authors and funding
8 authors.
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Abstract
Aberrant metabolic enzymes drive glucose metabolism reprogramming, which plays a crucial role in tumor malignancy and metastasis. Protein acetylation is one of the key regulatory mechanisms of metabolic enzyme function, yet its precise role requires further clarification. In the present study, we reported that the deacetylation and low expression of transaldolase 1 (TALDO1) mediated by HDAC6 weakened the inhibitory effect of TALDO1 on tumor proliferation and metastasis in nasopharyngeal carcinoma (NPC). Mechanistically, highly expressed HDAC6 induced lysine 7 (K7) deacetylation of TALDO1, which could inhibit SMURF1-mediated K63-linked ubiquitination, thus reducing the protein stability of TALDO1. Notably, TALDO1 deacetylation inhibited its nuclear translocation and interaction with BRCA1, thereby reducing the inhibition of c-Myc transcriptional activation, promoting the expression of HK2/LDHA/PDK1, and further enhancing glycolysis independent of TALDO1 enzyme activity. This research elucidated the regulatory mechanism of TALDO1 from the perspective of acetylation modification, clarified the moonlighting functions of TALDO1 in metabolic reprogramming, and provided novel biomarkers and intervention strategies, such as HDAC inhibitors, for the clinical treatment of NPC.
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