ArticleSignal transduction and targeted therapy2020
Insulin-like growth factor 1-induced enolase 2 deacetylation by HDAC3 promotes metastasis of pancreatic cancer.
Article in Signal transduction and targeted therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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85 citing papers in PubMed, 126 citations in OpenAlex.
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- Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026Review
- Aberrant sialylation in cancer: From molecular mechanisms to potential therapeutics.Genes & diseases · 2026Review
- Histone deacetylases in cancer metabolic reprogramming.Experimental & molecular medicine · 2026Review
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- ENO2 sustains cancer stemness and metastatic competence through a phosphoenolpyruvate-dependent metabolic axis in triple-negative breast cancer.Cell death & disease · 2026Article
- ENO2 drives tumor cell-induced M2 macrophage polarization to promote colorectal cancer liver metastasis.Signal transduction and targeted therapy · 2026Article
- Bottom-Up Programming of Cell States in Cancer Organoids with Defined Synthetic Adhesion Cues.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Impact of good glycemic control on survival of pancreatic ductal adenocarcinoma with diabetes mellitus.BMC gastroenterology · 2026Article
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- Reversible acetylation of Hpo regulates the Hippo pathway.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Mechanistic insights into hepatic metastasis of pancreatic cancer: molecular perspectives.Translational gastroenterology and hepatology · 2026Review
- Epigenomic and Metabolic Interplay in the Development of Metastatic Brain Tumors.Oncology research · 2026Review
- HDAC3-driven immunometabolic reprogramming in type 2 diabetes and its complications: from enzymatic deacetylation to non-enzymatic scaffolding.Frontiers in immunology · 2026Review
- A signature constructed with circadian rhythm-related genes to predict the prognosis and therapy response for low-grade gliomas.Discover oncology · 2025Article
- Cysteine-S-nitrosylation inhibits Rop5-mediated immune evasion inbioRxiv : the preprint server for biology · 2025Article
- Distinct microRNA profiles in neuron-derived extracellular vesicles between recent-onset and chronic-phase schizophrenia.Schizophrenia (Heidelberg, Germany) · 2025Article
- HDAC1/2-mediated deacetylation of KLF9 promotes the malignant progression of nasopharyngeal carcinoma via CDH17.Oncogene · 2025Article
- Low-Dose Quercetin Dephosphorylates AKT and Suppresses Proteins Related to Migration in Human Metastatic Uveal Melanoma Cells.Life (Basel, Switzerland) · 2025Article
- Knockdown of MACC1 expression attenuates colorectal cancer cell glucose metabolism by suppressing GLUT4 membrane translocation.Cancer biomarkers : section A of Disease markers · 2025Article
25 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Enolase 2 (ENO2) is a key glycolytic enzyme in the metabolic process of glycolysis, but its potential function in pancreatic ductal adenocarcinoma (PDAC) is unclear. In this study, we observed a significant overexpression of ENO2 in PDAC tissues, and its expression was correlated with metastasis and poor prognosis in PDAC patients. K394 was identified as a major acetylation site in ENO2 that regulates its enzymatic activity, cell metabolism and PDAC progression. Knockdown of ENO2 suppressed tumor growth and liver metastasis in PDAC. Re-expression of wild-type (WT) ENO2, but not the K394 acetylation mimetic mutant, could reverse the decreased tumor malignancy. We further characterized histone deacetylase 3 (HDAC3) and P300/CBP-associated factor (PCAF) as the potential deacetylase and acetyltransferase for ENO2, respectively. HDAC3-mediated deacetylation was shown to lead to ENO2 activation and enhancement of glycolysis. Importantly, insulin-like growth factor-1 (IGF-1) was found to decrease K394 acetylation and stimulate ENO2 activity in a dose- and time-dependent manner. The PI3K/AKT/mTOR pathway facilitated the phosphorylation of HDAC3 on S424, which promoted K394 deacetylation and activation of ENO2. Linsitinib, an oral small-molecule inhibitor of IGF-1R, could inhibit IGF-1-induced ENO2 deacetylation by HDAC3 and the PI3K/AKT/mTOR pathway. Furthermore, linsitinib showed a different effect on the growth and metastasis of PDAC depending on the overexpression of WT versus K394-mutant ENO2. Our results reveal a novel mechanism by which acetylation negatively regulates ENO2 activity in the metastasis of PDAC by modulating glycolysis. Blockade of IGF-1-induced ENO2 deacetylation represents a promising strategy to prevent the development of PDAC.
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