ArticleOncogene2020
HDAC8 promotes the dissemination of breast cancer cells via AKT/GSK-3β/Snail signals.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Histone modification of endothelial-mesenchymal transition in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022Pooled it
- Osthole attenuates cartilage degradation and chondrocyte pyroptosis in knee osteoarthritis and is associated with activation of the PI3K/Akt pathway.Molecular biology reports · 2026Article
- Asiatic acid promotes CD8Acta pharmacologica Sinica · 2026Article
- HDAC8 inhibition targets STAT3-MYC axis and synergizes with Venetoclax in KMT2A-rearranged acute myeloid leukemia.Leukemia · 2026Article
- Natural Products Targeting Acetylation in Bladder Cancer: Mechanistic Basis, Therapeutic Potential, and Future Perspectives.Current issues in molecular biology · 2026Review
- FAM83D facilitates EMT and metastasis of cervical cancer via interaction with GSK3β and inactivation of GSK3β/stabilization of Snail signaling.Biology direct · 2026Article
- Largazole targets Musashi protein expression via miR-125b-5p and sensitizes triple-negative breast cancer cells to radiation.Frontiers in pharmacology · 2026Article
- Targeted Degradation of Histone Deacetylase 8 Using Proteolysis Targeting Chimeras Technology: A Promising Approach for Glioblastoma Treatment.Drug design, development and therapy · 2026Article
- Recent progress in synthetic strategies to develop potent, HDAC8-selective, small-molecule inhibitors.Bioorganic & medicinal chemistry letters · 2025Review
- CK2B Induces CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Histone acetylation modulators in breast cancer.Breast cancer research : BCR · 2025Review
- Decoding the Epigenome of Breast Cancer.International journal of molecular sciences · 2025Review
- Stemness of Cancer: A Study of Triple-negative Breast Cancer From a Neuroscience Perspective.Stem cell reviews and reports · 2025Review
- Acetylation-Mediated Epigenetic Consequences for Biological Control and Cancer.Results and problems in cell differentiation · 2025Review
- Mechanisms of HDACs in cancer development.Frontiers in immunology · 2025Review
- The role of acetylation and deacetylation in cancer metabolism.Clinical and translational medicine · 2025Review
- Dissecting the epigenetic orchestra of HDAC isoforms in breast cancer development: a review.Medical oncology (Northwood, London, England) · 2024Review
- Discovery of a Highly Potent and Selective HDAC8 Degrader: Advancing the Functional Understanding and Therapeutic Potential of HDAC8.Journal of medicinal chemistry · 2024Article
- HDAC3 and HDAC8 PROTAC dual degrader reveals roles of histone acetylation in gene regulation.Cell chemical biology · 2023Article
- Targeting Histone Deacetylases 6 in Dual-Target Therapy of Cancer.Pharmaceutics · 2023Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanistic action of histone deacetylase 8 (HDAC8) in cancer motility, including epithelial-mesenchymal transition (EMT), remains largely undefined. We found that the expression of HDAC8 was upregulated in breast cancer (BC) cells and tissues as compared to the controls. Further, BC tissues had the highest values of HDAC8 expression among 31 kinds of cancers. Cellular study indicated that HDAC8 can positively regulate the dissemination and EMT of BC cells. It increased the protein stability of Snail, an important regulator of EMT, by phosphorylation of its motif 2 in serine-rich regions. There are 21 factors that have been reported to regulate the protein stability of Snail. Among them, HDAC8 can decrease the expression of GSK-3β through increasing its Ser9-phosphorylation. Mass spectrum analysis indicated that HDAC8 interact with AKT1 to decrease its acetylation while increase its phosphorylation, which further increased Ser9-phosphorylation of GSK-3β. The C-terminal of AKT1 was responsible for the interaction between HDAC8 and AKT1. Further, Lys426 was the key residue for HDAC8-regulated deacetylation of AKT1. Moreover, HDAC8/Snail axis acted as adverse prognosis factors for in vivo progression and overall survival (OS) rate of BC patients. Collectively, we found that HDAC8 can trigger the dissemination of BC cells via AKT/GSK-3β/Snail signals, which imposed that inhibition of HDAC8 is a potential approach for BC treatment.
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