ArticleThe Journal of biological chemistry2011
Histone deacetylase inhibitor belinostat represses survivin expression through reactivation of transforming growth factor beta (TGFbeta) receptor II leading to cancer cell death.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Epigenetic marvels: exploring the landscape of colorectal cancer treatment through cutting-edge epigenetic-based drug strategies.Clinical epigenetics · 2025Review
- Emerging Role of Epigenetic Modifiers in Breast Cancer Pathogenesis and Therapeutic Response.Cancers · 2023Review
- Epigenetic targets in B- and T-cell lymphomas: latest developments.Therapeutic advances in hematology · 2023Review
- Recent Update of HDAC Inhibitors in Lymphoma.Frontiers in cell and developmental biology · 2020Review
- MEF-2 isoforms' (A-D) roles in development and tumorigenesis.Oncotarget · 2019Review
- Histone Deacetylases (HDACs) Guided Novel Therapies for T-cell lymphomas.International journal of medical sciences · 2019Review
- Drugs Targeting Epigenetic Modifications and Plausible Therapeutic Strategies Against Colorectal Cancer.Frontiers in pharmacology · 2019Review
- Survivin, a molecular target for therapeutic interventions in squamous cell carcinoma.Cellular & molecular biology letters · 2017Review
- Suberoylanilide hydroxamic acid (SAHA) and cladribine synergistically induce apoptosis in NK-LGL leukaemia.British journal of haematology · 2015Article
- Belinostat: first global approval.Drugs · 2014Article
- Ezrin expression and cell survival regulation in colorectal cancer.Cellular signalling · 2014Article
- Akt inhibitor MK-2206 promotes anti-tumor activity and cell death by modulation of AIF and Ezrin in colorectal cancer.BMC cancer · 2014Article
- Targeting survivin in cancer: novel drug development approaches.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2014Review
- Inhibition of autophagy induced by TSA sensitizes colon cancer cell to radiation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- In vivo analysis of insulin-like growth factor type 1 receptor humanized monoclonal antibody MK-0646 and small molecule kinase inhibitor OSI-906 in colorectal cancer.Oncology reports · 2014Article
- Nanoparticles for urothelium penetration and delivery of the histone deacetylase inhibitor belinostat for treatment of bladder cancer.Nanomedicine : nanotechnology, biology, and medicine · 2013Article
- Differential PKA activation and AKAP association determines cell fate in cancer cells.Journal of molecular signaling · 2013Article
- Cell survival and metastasis regulation by Akt signaling in colorectal cancer.Cellular signalling · 2013Review
- The plasma membrane transporter SLC5A8 suppresses tumour progression through depletion of survivin without involving its transport function.The Biochemical journal · 2013Article
- Establishment and Validation of an Orthotopic Metastatic Mouse Model of Colorectal Cancer.ISRN hepatology · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Survivin is a cancer-associated gene that functions to promote cell survival, cell division, and angiogenesis and is a marker of poor prognosis. Histone deacetylase inhibitors induce apoptosis and re-expression of epigenetically silenced tumor suppressor genes in cancer cells. In association with increased expression of the tumor suppressor gene transforming growth factor β receptor II (TGFβRII) induced by the histone deacetylase inhibitor belinostat, we observed repressed survivin expression. We investigated the molecular mechanisms involved in survivin down-regulation by belinostat downstream of reactivation of TGFβ signaling. We identified two mechanisms. At early time points, survivin protein half-life was decreased with its proteasomal degradation. We observed that belinostat activated protein kinase A at early time points in a TGFβ signaling-dependent mechanism. After longer times (48 h), survivin mRNA was also decreased by belinostat. We made the novel observation that belinostat mediated cell death through the TGFβ/protein kinase A signaling pathway. Induction of TGFβRII with concomitant survivin repression may represent a significant mechanism in the anticancer effects of this drug. Therefore, patient populations exhibiting high survivin expression with epigenetically silenced TGFβRII might potentially benefit from the use of this histone deacetylase inhibitor.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.