ArticleClinical cancer research : an official journal of the American Association for Cancer Research2007
Synergistic interactions between vorinostat and sorafenib in chronic myelogenous leukemia cells involve Mcl-1 and p21CIP1 down-regulation.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 65 citations in OpenAlex.
- Phase I/II trial of vorinostat, bevacizumab, and daily temozolomide for recurrent malignant gliomas.Journal of neuro-oncology · 2018Trial
- Mcl-1 dependence predicts response to vorinostat and gemtuzumab ozogamicin in acute myeloid leukemia.Leukemia research · 2014Trial
- Synergistic Activity of N-hydroxy-7-(2-naphthylthio) Heptanomide and Sorafenib Against Cancer Stem Cells, Anaplastic Thyroid Cancer.Neoplasia (New York, N.Y.) · 2017Article
- ABT-263 enhances sorafenib-induced apoptosis associated with Akt activity and the expression of Bax and p21((CIP1/WAF1)) in human cancer cells.British journal of pharmacology · 2014Article
- Synergistic interaction between the HDAC inhibitor, MPT0E028, and sorafenib in liver cancer cells in vitro and in vivo.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Connexin-dependent gap junction enhancement is involved in the synergistic effect of sorafenib and all-trans retinoic acid on HCC growth inhibition.Oncology reports · 2014Article
- A phase I study of sorafenib and vorinostat in patients with advanced solid tumors with expanded cohorts in renal cell carcinoma and non-small cell lung cancer.Investigational new drugs · 2013Article
- PLK1 inhibitors synergistically potentiate HDAC inhibitor lethality in imatinib mesylate-sensitive or -resistant BCR/ABL+ leukemia cells in vitro and in vivo.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
- EVI1 inhibits apoptosis induced by antileukemic drugs via upregulation of CDKN1A/p21/WAF in human myeloid cells.PloS one · 2013Article
- Synergistic growth inhibition by sorafenib and vitamin K2 in human hepatocellular carcinoma cells.Clinics (Sao Paulo, Brazil) · 2012Article
- Sorafenib: complexities of Raf-dependent and Raf-independent signaling are now unveiled.Medical molecular morphology · 2011Review
- Vitamin K enhancement of sorafenib-mediated HCC cell growth inhibition in vitro and in vivo.International journal of cancer · 2010Article
- Deactylase inhibition in myeloproliferative neoplasms.Investigational new drugs · 2010Review
- Vorinostat and sorafenib increase CD95 activation in gastrointestinal tumor cells through a Ca(2+)-de novo ceramide-PP2A-reactive oxygen species-dependent signaling pathway.Cancer research · 2010Article
- Sorafenib activates CD95 and promotes autophagy and cell death via Src family kinases in gastrointestinal tumor cells.Molecular cancer therapeutics · 2010Article
- Sorafenib combined vitamin K induces apoptosis in human pancreatic cancer cell lines through RAF/MEK/ERK and c-Jun NH2-terminal kinase pathways.Journal of cellular physiology · 2010Article
- Deacetylase inhibitors - focus on non-histone targets and effects.World journal of biological chemistry · 2010Article
- Endogenous Bak inhibitors Mcl-1 and Bcl-xL: differential impact on TRAIL resistance in Bax-deficient carcinoma.The Journal of cell biology · 2010Article
- Epigenetic therapies for chemoresensitization of epithelial ovarian cancer.Gynecologic oncology · 2010Review
- Sorafenib and vorinostat kill colon cancer cells by CD95-dependent and -independent mechanisms.Molecular pharmacology · 2009Article
Corrections and comments
- Retraction · 2016-10-01Falsification/Fabrication of Data · Falsification/Fabrication of Image · Investigation by ORI · Misconduct by Author ·
- Commented on by
- Commented on by
- Retracted
Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
Abstract
purposeInteractions between the multikinase inhibitor sorafenib (Bay 43-9006) and the histone deacetylase inhibitor vorinostat were examined in chronic myelogenous leukemia (CML) cells sensitive and resistant to imatinib mesylate. EXPERIMENTAL
designK562, LAMA 84, and primary CML patient-derived CD34(+) mononuclear cells were exposed to vorinostat followed by sorafenib, after which effects on cell viability and various survival signaling pathways were monitored by flow cytometry, clonogenic assays, and Western blotting. Real-time reverse transcription-PCR was used to monitor gene expression, and the functional contribution of p21(CIP1) and Mcl-1 down-regulation were determined in cells transfected with corresponding constructs.
resultsPretreatment (24 h) with vorinostat followed by sorafenib optimally induced mitochondrial injury and cell death in Bcr/Abl(+) cells (e.g., K562 and LAMA 84). Similar results were obtained in imatinib mesylate-resistant cells expressing activated Lyn as well as in primary CD34(+) bone marrow cells obtained from CML patients. This regimen also markedly inhibited CML cell colony formation. Combined but not individual treatment of CML cells with vorinostat and sorafenib triggered pronounced mitochondrial dysfunction (i.e., cytochrome c, Smac, and AIF release), caspase activation, poly(ADP-ribose) polymerase cleavage, and down-regulation of Mcl-1. Sorafenib also blocked vorinostat-mediated induction of p21(CIP1). Down-regulation of Mcl-1 was caspase and transcription independent, whereas p21(CIP1) down-regulation was partially caspase and transcription dependent. Enforced expression of p21(CIP1) and particularly Mcl-1 significantly attenuated vorinostat/sorafenib-mediated lethality.
conclusionsThese findings suggest that combined treatment with vorinostat and sorafenib synergistically induces apoptosis in CML cells through a process that involves Mcl-1 down-regulation and inhibition of p21(CIP1) induction.
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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.