ArticleEMBO molecular medicine2018
Dual inhibition of AKT-mTOR and AR signaling by targeting HDAC3 in
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Article in EMBO molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36citing papers in PubMed
5.9field-weighted citation impact, top 3% of its field
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Who cites it
36 citing papers in PubMed, 51 citations in OpenAlex.
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- CXCR2 blockade potentiates HDAC3 deletion mediated antitumor immunity in colorectal cancer.Cell death & disease · 2026Article
- CRISPR Screen Identifies HDAC3 as a Novel Radiosensitizing Target in Small Cell Lung Cancer.Molecular cancer therapeutics · 2026Article
- KBTBD11 loss promotes AKT hyperactivation and therapeutic vulnerability in prostate cancer.Oncogene · 2025Article
- Harnessing organoid technology in urological cancer: advances and applications in urinary system tumors.World journal of surgical oncology · 2025Review
- Differential regulation of mTORC2 signalling by type I and type II calreticulin (CALR) driver mutations of myeloproliferative neoplasm.Cell communication and signaling : CCS · 2025Article
- The role of acetylation and deacetylation in cancer metabolism.Clinical and translational medicine · 2025Review
- HDAC3 inhibitors induce drug resistance by promoting IL-17 A production by T cells.Scientific reports · 2024Article
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- TORSEL, a 4EBP1-based mTORC1 live-cell sensor, reveals nutrient-sensing targeting by histone deacetylase inhibitors.Cell & bioscience · 2024Article
- Addressing the Reciprocal Crosstalk between the AR and the PI3K/AKT/mTOR Signaling Pathways for Prostate Cancer Treatment.International journal of molecular sciences · 2023Review
- Valeric acid acts as a novel HDAC3 inhibitor against prostate cancer.Medical oncology (Northwood, London, England) · 2022Article
- Valeric acid acts as a novel HDAC3 inhibitor against prostate cancer.Medical oncology (Northwood, London, England) · 2022Article
- Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022Review
- PTEN loss promotes Warburg effect and prostate cancer cell growth by inducing FBP1 degradation.Frontiers in oncology · 2022Article
- GLI3 Is Stabilized by SPOP Mutations and Promotes Castration Resistance via Functional Cooperation with Androgen Receptor in Prostate Cancer.Molecular cancer research : MCR · 2022Article
- Transcription factor 3 (TCF3) combined with histone deacetylase 3 (HDAC3) down-regulates microRNA-101 to promote Burkitt lymphoma cell proliferation and inhibit apoptosis.Bioengineered · 2021Article
- Vorinostat (SAHA) and Breast Cancer: An Overview.Cancers · 2021Review
- Functional genomics approaches to improve pre-clinical drug screening and biomarker discovery.EMBO molecular medicine · 2021Review
- KDELR2 promotes breast cancer proliferation via HDAC3-mediated cell cycle progression.Cancer communications (London, England) · 2021Article
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Authors and funding
25 authors at 5 institutions in 2 countries.
Yuqian YanDepartment of Gastroenterology, Jiangxi Institute of Gastroenterology and Hepatology, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Jian AnDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Yinhui YangDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Di WuDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Yang BaiDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
William CaoDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Linlin MaDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Junhui ChenDepartment of Minimally Invasive Intervention, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Zhendong YuCentral Laboratory, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Yundong HeDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Xin JinDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Yunqian PanDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Tao MaDepartment of Biomedical Statistics and Informatics, Mayo Clinic Cancer Center, Rochester, MN, USA.
Shangqian WangHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Xiaonan HouDepartment of Oncology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Saravut John WerohaDepartment of Oncology, Mayo Clinic College of Medicine, Rochester, MN, USA.
R Jeffrey KarnesDepartment of Urology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Jun ZhangDepartment of Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Jennifer J WestendorfDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Liguo WangDepartment of Biomedical Statistics and Informatics, Mayo Clinic Cancer Center, Rochester, MN, USA.
Yu ChenHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Wanhai XuDepartment of Urology, The Fourth Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Runzhi ZhuCenter for Cell Therapy, The Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China runzhizhu1978@163.com wdj5257@sina.com huang.haojie@mayo.edu.ORCID 0000-0002-9565-7261
Dejie WangDepartment of Gastroenterology, Jiangxi Institute of Gastroenterology and Hepatology, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China runzhizhu1978@163.com wdj5257@sina.com huang.haojie@mayo.edu.ORCID 0000-0003-3870-2385
Haojie HuangDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA runzhizhu1978@163.com wdj5257@sina.com huang.haojie@mayo.edu.ORCID 0000-0003-2751-6413
Mayo Clinic · USJiangsu University · CNMemorial Sloan Kettering Cancer Center · USPeking University Shenzhen Hospital · CNHarbin Medical University · CN
Funding
X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4MSPORE In Prostate CancerP50CA092629 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Yu Chen, MICHAEL J MORRIS · 2001 to 2026
$63.0MThe MSKCC-UW/Fred Hutch Prostate Cancer Drug Resistance and Sensitivity CenterU54CA224079 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SAWYERS, CHARLES L. · 2017 to 2021
$6.8MRole of ETS factors in specifying prostate luminal cell identity and androgen receptor dependenceR01CA193837 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SAWYERS, CHARLES L. · 2015 to 2025
$4.7MRole of proinflammatory cytokine-induced AR degradation in castration-resistant prostate cancerR01CA130908 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI HUANG, HAOJIE · 2010 to 2021
$3.5MRole of FOXO1 Inactivation in Prostate TumorigenesisR01CA134514 · NCI · UNIVERSITY OF MINNESOTA · PI HUANG, HAOJIE · 2009 to 2019
$3.3MUnderstanding the role of an aberrant hepatic nuclear transcription circuit in prostate cancer tumorigenesis and castration resistanceR01CA208100 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI CHEN, YU · 2017 to 2021
$2.5MRole of RUNX2 in prostate cancer intratumoral androgen synthesis and progressionR01CA193239 · NCI · MAYO CLINIC ROCHESTER · PI HUANG, HAOJIE · 2015 to 2019
$1.8MNCI NIH HHS P30 CA008748NCI NIH HHS P50 CA092629NCI NIH HHS R01 CA130908NCI NIH HHS R01 CA134514NCI NIH HHS R01 CA193239NCI NIH HHS R01 CA193837NCI NIH HHS R01 CA208100NCI NIH HHS U54 CA224079
Abstract
AKT-mTOR and androgen receptor (AR) signaling pathways are aberrantly activated in prostate cancer due to frequent PTEN deletions or SPOP mutations. A clinical barrier is that targeting one of them often activates the other. Here, we demonstrate that HDAC3 augments AKT phosphorylation in prostate cancer cells and its overexpression correlates with AKT phosphorylation in patient samples. HDAC3 facilitates lysine-63-chain polyubiquitination and phosphorylation of AKT, and this effect is mediated by AKT deacetylation at lysine 14 and 20 residues and HDAC3 interaction with the scaffold protein APPL1. Conditional homozygous deletion of
Indexed as
AcrylamidesAnimalsBlotting, WesternGenotypeHEK293 CellsHistone Deacetylase 3Histone DeacetylasesHumansImmunoprecipitationMaleMiceMice, KnockoutNuclear ProteinsPhenylenediaminesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseAcrylamidesHistone Deacetylase 3Histone DeacetylasesNuclear ProteinsPhenylenediaminesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseReceptors, AndrogenRepressor ProteinsRGFP966SPOP protein, humanSpop protein, mouseTOR Serine-Threonine KinasesUbiquitin-Protein Ligase ComplexesAKT phosphorylationandrogen receptorHDAC3prostate cancerRGFP966
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