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Cited by 13Histone Deacetylase Inhibitors ResearchGlioma Diagnosis and TreatmentEpigenetics and DNA Methylation

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A novel histone deacetylase inhibitor, CKD5, has potent anti-cancer effects in glioblastoma

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Choi, Seung Ah, Kwak, Pil Ae, Park, Chul-Kee, Wang, Kyu-Chang, Phi, Ji Hoon, Lee, Ji Yeoun, Lee, Chang Sik, Lee, Ju-Hee, Kim, Seung-Ki·2017·Oncotarget
DOI 10.18632/oncotarget.13265PMC PMC5354719
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Abstract

// Seung Ah Choi 1, 2 , Pil Ae Kwak 1, 2 , Chul-Kee Park 3 , Kyu-Chang Wang 1, 3 , Ji Hoon Phi 1, 2, 3 , Ji Yeoun Lee 1, 3, 4 , Chang Sik Lee 5 , Ju-Hee Lee 5 , Seung-Ki Kim 1, 2, 3 1 Division of Pediatric Neurosurgery, Pediatric Clinical Neuroscience Center, Seoul National University Children’s Hospital, Seoul, Korea 2 Adolescent Cancer Center, Seoul National University Cancer Hospital, Seoul, Korea 3 Department of Neurosurgery, Seoul National University Hospital, Seoul, Korea 4 Department of Anatomy, Seoul National University Hospital, Seoul, Korea 5 Chong Kun Dang Research Institute, CKD Pharmaceuticals, Gyeonggi-do, Korea Correspondence to: Seung-Ki Kim, email: nsthomas@snu.ac.kr Keywords: epigenetics, histone deacetylase inhibitor, glioblastoma Received: May 09, 2016 Accepted: November 01, 2016 Published: November 10, 2016 ABSTRACT There have been extensive efforts to improve the outcome of glioblastoma, but the prognosis of this disease has not been significantly altered to date. Histone deacetylase inhibitors (HDACIs) have been evaluated as promising anti-cancer drugs and regulate cell growth, cell cycle arrest and apoptosis in glioblastoma. Here, we demonstrated the therapeutic efficacy of a novel pan-HDACI, 7-ureido-N-hydroxyheptanamide derivative (CKD5), compared with traditional pan-HDACIs, such as suberoylanilide hydroxamic acid (SAHA) and trichostatin A (TSA), in vitro and in vivo . Compared with SAHA and TSA, CKD5 had improved cytotoxic effects and induced apoptosis, anti-proliferative activity and cell cycle arrest at G2/M phase. Furthermore, CKD5 significantly reduced tumor volume and prolonged the survival in vivo compared with TSA, suggesting improved anti-cancer efficacy among HDACIs. Our results demonstrate that the novel HDACI CKD5 is a promising therapeutic candidate for glioblastoma.

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  • HDAC inhibitor SAHA shows strong effects in destabilizing mut-p53 by dissociating HDAC6 from functional interaction with Hsp90 and thereby inhibits glioblastoma growth and resistance to chemotherapy.

    “HDAC inhibitor SAHA shows strong effects in destabilizing mut-p53 by dissociating HDAC6 from functional interaction with Hsp90 and thereby inhibits GBM growth and resistance to chemotherapy [142,143,144,145,146].”

    From The p53 Pathway in Glioblastoma (2018) · cites this paper as [145]

    The Results section reports that SAHA suppressed glioblastoma cell growth, and the Discussion identifies SAHA as an HDAC6 inhibitor. The paper does not report mutant-p53 destabilization, disruption of an HDAC6–Hsp90 interaction, or reduced chemotherapy resistance. Its Discussion also describes SAHA’s clinical effect in glioblastoma as modest. Page numbers are not available in our copy. (LLM, conf=0.88)

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Research works printed but not linked: 42

  1. Kesari, 2008, Malignant gliomas in adults, N Engl J Med, 359, 492, 10.1056/NEJMra0708126 · DOI · Paper page
  2. Banik, 2012, Drug resistance in glioblastoma: a mini review, Neurochem Res, 37, 1192, 10.1007/s11064-011-0701-1 · DOI
  3. Rich, 2007, Molecularly targeted therapy for malignant glioma, Cancer, 110, 13, 10.1002/cncr.22741 · DOI
  4. Gijtenbeek, 2009, Effects of radiotherapy with concomitant and adjuvant temozolomide versus radiotherapy alone on survival in glioblastoma in a randomised phase III study: 5-year analysis of the EORTC-NCIC trial, Lancet Oncol, 10, 459, 10.1016/S1470-2045(09)70025-7 · DOI
  5. Pelicci, 2006, Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer, Nat Rev Cancer, 6, 38, 10.1038/nrc1779 · DOI
  6. Naumann, 2013, HDAC inhibitors and their potential applications to glioblastoma therapy, Oncoimmunology, 2, e25219, 10.4161/onci.25219 · DOI
  7. Liu, 2013, HDAC inhibitor DWP0016 activates p53 transcription and acetylation to inhibit cell growth in U251 glioblastoma cells, J Cell Biochem, 114, 1498, 10.1002/jcb.24491 · DOI
  8. Das, 2015, Mechanisms and clinical significance of histone deacetylase inhibitors: epigenetic glioblastoma therapy, Anticancer Res, 35, 615
  9. Chandra, 2015, Preclinical activity of combined HDAC and KDM1A inhibition in glioblastoma, Neuro Oncol, 17, 1463, 10.1093/neuonc/nov041 · DOI
  10. Chandra, 2011, Inhibition of LSD1 sensitizes glioblastoma cells to histone deacetylase inhibitors, Neuro Oncol, 13, 894, 10.1093/neuonc/nor049 · DOI
  11. Culf, 2014, Metabolic Effects of Known and Novel HDAC and SIRT Inhibitors in Glioblastomas Independently or Combined with Temozolomide, Metabolites, 4, 807, 10.3390/metabo4030807 · DOI
  12. Bezecny, 2014, Histone deacetylase inhibitors in glioblastoma: pre-clinical and clinical experience, Med Oncol, 31, 985, 10.1007/s12032-014-0985-5 · DOI
  13. Merlo, 2008, Histone deacetylase inhibition and blockade of the glycolytic pathway synergistically induce glioblastoma cell death, Clin Cancer Res, 14, 3132, 10.1158/1078-0432.CCR-07-4182 · DOI
  14. Haas-Kogan, 2007, In vivo efficacy of a novel histone deacetylase inhibitor in combination with radiation for the treatment of gliomas, Neuro Oncol, 9, 82, 10.1215/15228517-2006-032 · DOI
  15. Ramos, 2014, The promise and failures of epigenetic therapies for cancer treatment, Cancer Treat Rev, 40, 153, 10.1016/j.ctrv.2013.05.009 · DOI
  16. Llovera, 2014, Histone deacetylase inhibitors promote glioma cell death by G2 checkpoint abrogation leading to mitotic catastrophe, Cell Death Dis, 5, e1435, 10.1038/cddis.2014.412 · DOI
  17. Grundy, 2010, Histone deacetylase inhibition attenuates cell growth with associated telomerase inhibition in high-grade childhood brain tumor cells, Mol Cancer Ther, 9, 2568, 10.1158/1535-7163.MCT-10-0272 · DOI
  18. Naumann, 2013, The histone deacetylase inhibitor trichostatin a promotes apoptosis and antitumor immunity in glioblastoma cells, Anticancer Res, 33, 1351
  19. Bae, 2006, Trichostatin A increases the thermosensitivity of human glioblastoma A172 cells, Neurosci Lett, 396, 230, 10.1016/j.neulet.2005.11.041 · DOI
  20. Chen, 2011, NBM-HD-3, a novel histone deacetylase inhibitor with anticancer activity through modulation of PTEN and AKT in brain cancer cells, J Ethnopharmacol, 136, 156, 10.1016/j.jep.2011.04.034 · DOI
  21. Chen, 2006, Antitumor effects of a novel phenylbutyrate-based histone deacetylase inhibitor, (S)-HDAC-42, in prostate cancer, Clin Cancer Res, 12, 5199, 10.1158/1078-0432.CCR-06-0429 · DOI
  22. Richon, 2002, The histone deacetylase inhibitor SAHA arrests cancer cell growth, up-regulates thioredoxin-binding protein-2, and down-regulates thioredoxin, Proc Natl Acad Sci U S A, 99, 11700, 10.1073/pnas.182372299 · DOI
  23. Park, 2009, A novel delta-lactam-based histone deacetylase inhibitor, KBH-A42, induces cell cycle arrest and apoptosis in colon cancer cells, Biochem Pharmacol, 78, 486, 10.1016/j.bcp.2009.05.010 · DOI
  24. Bae, 2011, Histone deacetylase inhibitors: molecular mechanisms of action and clinical trials as anti-cancer drugs, Am J Transl Res, 3, 166
  25. Park, 2006, Trichostatin A induces apoptosis in lung cancer cells via simultaneous activation of the death receptor-mediated and mitochondrial pathway?, Exp Mol Med, 38, 616, 10.1038/emm.2006.73 · DOI
  26. Chen, 2007, The HDAC inhibitor trichostatin A inhibits growth of small cell lung cancer cells, J Surg Res, 142, 219, 10.1016/j.jss.2006.12.555 · DOI
  27. Martinez, 2012, Differential response of cancer cells to HDAC inhibitors trichostatin A and depsipeptide, Br J Cancer, 106, 116, 10.1038/bjc.2011.532 · DOI
  28. Chinnaiyan, 2010, Vorinostat enhances the cytotoxic effects of the topoisomerase I inhibitor SN38 in glioblastoma cell lines, J Neurooncol, 99, 201, 10.1007/s11060-010-0127-7 · DOI
  29. Tallen, 2010, The inhibitor of growth 1 (ING1) is involved in trichostatin A-induced apoptosis and caspase 3 signaling in p53-deficient glioblastoma cells, Oncol Res, 18, 469
  30. Eyupoglu, 2014, Histone deacetylases inhibition by SAHA/Vorinostat normalizes the glioma microenvironment via xCT equilibration, Sci Rep, 4, 6226, 10.1038/srep06226 · DOI
  31. Sharma, 2014, Histone deacetylase inhibitors trichostatin A and vorinostat inhibit TGFbeta2-induced lens epithelial-to-mesenchymal cell transition, Invest Ophthalmol Vis Sci, 55, 4731, 10.1167/iovs.14-14109 · DOI
  32. Giannini, 2009, Phase II trial of vorinostat in recurrent glioblastoma multiforme: a north central cancer treatment group study, J Clin Oncol, 27, 2052, 10.1200/JCO.2008.19.0694 · DOI
  33. Galanis, 2012, Phase II trial of vorinostat in combination with bortezomib in recurrent glioblastoma: a north central cancer treatment group study, Neuro Oncol, 14, 215, 10.1093/neuonc/nor198 · DOI
  34. Mittapalli, 2009, Vorinostat inhibits brain metastatic colonization in a model of triple-negative breast cancer and induces DNA double-strand breaks, Clin Cancer Res, 15, 6148, 10.1158/1078-0432.CCR-09-1039 · DOI
  35. Rizvi, 2009, Vorinostat in solid and hematologic malignancies, J Hematol Oncol, 2, 31, 10.1186/1756-8722-2-31 · DOI
  36. Andrews, 2010, Nonclinical safety assessment of the histone deacetylase inhibitor vorinostat, Int J Toxicol, 29, 3, 10.1177/1091581809352111 · DOI
  37. Lee, 2014, Panobinostat plus bortezomib and dexamethasone versus placebo plus bortezomib and dexamethasone in patients with relapsed or relapsed and refractory multiple myeloma: a multicentre, randomised, double-blind phase 3 trial, Lancet Oncol, 15, 1195, 10.1016/S1470-2045(14)70440-1 · DOI
  38. Palumbo, 2013, Vorinostat or placebo in combination with bortezomib in patients with multiple myeloma (VANTAGE 088): a multicentre, randomised, double-blind study, Lancet Oncol, 14, 1129, 10.1016/S1470-2045(13)70398-X · DOI
  39. Gore, 2007, Addition of histone deacetylase inhibitors in combination therapy, J Clin Oncol, 25, 1955, 10.1200/JCO.2006.09.8293 · DOI
  40. Kim, 2015, Disulfiram modulates stemness and metabolism of brain tumor initiating cells in atypical teratoid/rhabdoid tumors, Neuro Oncol, 17, 810, 10.1093/neuonc/nou305 · DOI
  41. Saito, 2013, Novel modified method for injection into the cerebrospinal fluid via the cerebellomedullary cistern in mice, Acta Neurobiol Exp (Wars), 73, 304, 10.55782/ane-2013-1938 · DOI
  42. Nedergaard, 2013, Paravascular microcirculation facilitates rapid lipid transport and astrocyte signaling in the brain, Sci Rep, 3, 2582, 10.1038/srep02582 · DOI

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Metadata

Authors
Choi, S. A., Kwak, P. A., Park, C.-K., Wang, K.-C., Phi, J. H., Lee, J. Y., Lee, C. S., Lee, J.-H., & Kim, S.-K.
Affiliations
  • Seoul National University (KR)
  • Chong Kun Dang Bio (South Korea) (KR)
ORCID
Venue
Oncotarget
Publisher
Impact Journals, LLC
Published
2016-11-10
Volume
8
Issue
6
Pages
9123-9133
ISSN
1949-2553 (ISSN-L)
DOI
10.18632/oncotarget.13265
PMC
PMC5354719
OpenAlex
W2549648494
Cited by
13
References
0
Citations by year
2025: 4 · 2024: 1 · 2023: 1 · 2021: 1 · 2020: 2 · 2019: 2 · 2018: 1 · 2017: 1
FWCI
0.69
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Oncotarget (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
  • Health Sciences › Medicine › Oncology › Glioma Diagnosis and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Keywords
histone deacetylase inhibitors, glioblastoma, vorinostat, trichostatin A, apoptosis, cell cycle arrest, G2/M cell cycle arrest, tumor growth inhibition, antiproliferative activity
MeSH terms
Vorinostat, Animals, Brain Neoplasms, Dose-Response Relationship, Drug, Female, Glioblastoma, Humans, Hydroxamic Acids, Mice, Inbred BALB C, Mice, Nude, Time Factors, Urea, Apoptosis, Xenograft Model Antitumor Assays, Cell Line, Tumor, Tumor Burden, Cell Proliferation, Histone Deacetylase Inhibitors, G2 Phase Cell Cycle Checkpoints

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