The novel NF-κB inhibitor DHMEQ synergizes with celecoxib to exert antitumor effects on human liver cancer cells by a ROS-dependent mechanism.
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[1] Verena Jendrossek,et al. Targeting apoptosis pathways by Celecoxib in cancer. , 2013, Cancer letters.
[2] J. McCubrey,et al. COX-2-dependent and COX-2-independent mode of action of celecoxib in human liver cancer cells. , 2011, Omics : a journal of integrative biology.
[3] Michael J Morgan,et al. Crosstalk of reactive oxygen species and NF-κB signaling , 2011, Cell Research.
[4] Wei Wang,et al. Combined Inhibitory Effects of Celecoxib and Fluvastatin on the Growth of Human Hepatocellular Carcinoma Xenografts in Nude Mice , 2010, The Journal of international medical research.
[5] P. Fisher,et al. Vorinostat and sorafenib increase CD95 activation in gastrointestinal tumor cells through a Ca(2+)-de novo ceramide-PP2A-reactive oxygen species-dependent signaling pathway. , 2010, Cancer research.
[6] P. Fisher,et al. 17-Allylamino-17-Demethoxygeldanamycin and MEK1/2 Inhibitors Kill GI Tumor Cells via Ca2+-Dependent Suppression of GRP78/BiP and Induction of Ceramide and Reactive Oxygen Species , 2010, Molecular Cancer Therapeutics.
[7] J. McCubrey,et al. Novel combination of Celecoxib and proteasome inhibitor MG132 provides synergistic antiproliferative and proapoptotic effects in human liver tumor cells , 2010, Cell cycle.
[8] A. Schönthal,et al. Enhanced killing of chemo-resistant breast cancer cells via controlled aggravation of ER stress. , 2009, Cancer letters.
[9] J. McCubrey,et al. Antitumor Effects of Dehydroxymethylepoxyquinomicin, a Novel Nuclear Factor-κB Inhibitor, in Human Liver Cancer Cells Are Mediated through a Reactive Oxygen Species-Dependent Mechanism , 2009, Molecular Pharmacology.
[10] T. Kasahara,et al. Celecoxib potently inhibits TNFalpha-induced nuclear translocation and activation of NF-kappaB. , 2008, Biochemical pharmacology.
[11] M. Kitamura,et al. Induction of apoptosis by cigarette smoke via ROS-dependent endoplasmic reticulum stress and CCAAT/enhancer-binding protein-homologous protein (CHOP). , 2008, Free radical biology & medicine.
[12] E. Reddy,et al. Celecoxib and a novel COX-2 inhibitor ON09310 upregulate death receptor 5 expression via GADD153/CHOP , 2008, Oncogene.
[13] R. Meacham,et al. Oxidative stress is inherent in prostate cancer cells and is required for aggressive phenotype. , 2008, Cancer research.
[14] M. Kitamura,et al. Involvement of Selective Reactive Oxygen Species Upstream of Proapoptotic Branches of Unfolded Protein Response* , 2008, Journal of Biological Chemistry.
[15] K. Oguchi,et al. Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells. , 2007, Toxicology.
[16] M. Cervello,et al. Potentiation of the antitumor effects of both selective cyclooxygenase-1 and cyclooxygenase-2 inhibitors in human hepatic cancer cells by inhibition of the MEK/ERK pathway , 2007, Cancer biology & therapy.
[17] J. Uddin,et al. Calcium-activated endoplasmic reticulum stress as a major component of tumor cell death induced by 2,5-dimethyl-celecoxib, a non-coxib analogue of celecoxib , 2007, Molecular Cancer Therapeutics.
[18] H. Nakamura,et al. Tumor-targeted induction of oxystress for cancer therapy , 2007, Journal of drug targeting.
[19] Y. Takeda,et al. Role of the Fas/FasL pathway in combination therapy with interferon-alpha and fluorouracil against hepatocellular carcinoma in vitro. , 2007, Journal of hepatology.
[20] B. Aggarwal,et al. Inflammation and cancer: how hot is the link? , 2006, Biochemical pharmacology.
[21] K. Eguchi,et al. DHMEQ, a novel NF-kappaB inhibitor, induces apoptosis and cell-cycle arrest in human hepatoma cells. , 2006, International journal of oncology.
[22] C. Trautwein,et al. Cyclooxygenase-2 inhibition induces apoptosis signaling via death receptors and mitochondria in hepatocellular carcinoma. , 2006, Cancer research.
[23] J. Uddin,et al. Downregulation of survivin expression and concomitant induction of apoptosis by celecoxib and its non-cyclooxygenase-2-inhibitory analog, dimethyl-celecoxib (DMC), in tumor cells in vitro and in vivo , 2006, Molecular Cancer.
[24] B. Gastman,et al. Interrelated Roles for Mcl-1 and BIM in Regulation of TRAIL-mediated Mitochondrial Apoptosis* , 2006, Journal of Biological Chemistry.
[25] P. Poma,et al. Antitumor effects of the novel NF-kappaB inhibitor dehydroxymethyl-epoxyquinomicin on human hepatic cancer cells: analysis of synergy with cisplatin and of possible correlation with inhibition of pro-survival genes and IL-6 production. , 2006, International journal of oncology.
[26] Amy S. Lee,et al. Stress induction of GRP78/BiP and its role in cancer. , 2006, Current molecular medicine.
[27] P. Galle,et al. Mcl-1 is an anti-apoptotic factor for human hepatocellular carcinoma. , 2006, International journal of oncology.
[28] H. Hayashi,et al. TRB3, a novel ER stress‐inducible gene, is induced via ATF4–CHOP pathway and is involved in cell death , 2005, The EMBO journal.
[29] P. Poma,et al. Induction of Apoptosis and Inhibition of Cell Growth in Human Hepatocellular Carcinoma Cells by COX‐2 Inhibitors , 2004, Annals of the New York Academy of Sciences.
[30] M. Labbozzetta,et al. Expression of WISPs and of Their Novel Alternative Variants in Human Hepatocellular Carcinoma Cells , 2004, Annals of the New York Academy of Sciences.
[31] H. Namba,et al. Induction of Thyroid Cancer Cell Apoptosis by a Novel Nuclear Factor κB Inhibitor, Dehydroxymethylepoxyquinomicin , 2004, Clinical Cancer Research.
[32] K. Umezawa,et al. Preparation and biological activities of optically active dehydroxymethylepoxyquinomicin, a novel NF-κB inhibitor , 2004 .
[33] Patrick Dumont,et al. Mitochondrial p53 activates Bak and causes disruption of a Bak–Mcl1 complex , 2004, Nature Cell Biology.
[34] A. Sirica,et al. Celecoxib‐induced apoptosis in rat cholangiocarcinoma cells mediated by Akt inactivation and Bax translocation , 2004, Hepatology.
[35] Yanan Yang,et al. Caspase-dependent apoptosis and -independent poly(ADP-ribose) polymerase cleavage induced by transforming growth factor beta1. , 2004, The international journal of biochemistry & cell biology.
[36] C. Chou,et al. DNA-damaging reagents induce apoptosis through reactive oxygen species-dependent Fas aggregation , 2003, Oncogene.
[37] P. Schirmacher,et al. Proapoptotic and antiproliferative potential of selective cyclooxygenase‐2 inhibitors in human liver tumor cells , 2002, Hepatology.
[38] Ping Liu,et al. Activation of NF-kappaB, AP-1 and STAT transcription factors is a frequent and early event in human hepatocellular carcinomas , 2002 .
[39] Pan‐Chyr Yang,et al. Cyclooxygenase-2 Inducing Mcl-1-dependent Survival Mechanism in Human Lung Adenocarcinoma CL1.0 Cells , 2001, The Journal of Biological Chemistry.
[40] C. Ong,et al. Role of intracellular thiol depletion, mitochondrial dysfunction and reactive oxygen species in Salvia miltiorrhiza-induced apoptosis in human hepatoma HepG2 cells. , 2001, Life sciences.
[41] M. Hengartner. The biochemistry of apoptosis , 2000, Nature.
[42] Guido Kroemer,et al. Mitochondrial control of cell death , 2000, Nature Medicine.
[43] A. Bowie,et al. Oxidative stress and nuclear factor-kappaB activation: a reassessment of the evidence in the light of recent discoveries. , 2000, Biochemical pharmacology.
[44] Junying Yuan,et al. Cleavage of BID by Caspase 8 Mediates the Mitochondrial Damage in the Fas Pathway of Apoptosis , 1998, Cell.
[45] K. Schulze-Osthoff,et al. Role of Reactive Oxygen Intermediates in Activation-induced CD95 (APO-1/Fas) Ligand Expression* , 1998, The Journal of Biological Chemistry.
[46] S. Krähenbühl,et al. Canalicular bile flow and bile salt secretion are maintained in rats with liver cirrhosis. Further evidence for the intact cell hypothesis. , 1988, Journal of hepatology.
[47] T. Chou,et al. Quantitative analysis of dose-effect relationships: the combined effects of multiple drugs or enzyme inhibitors. , 1984, Advances in enzyme regulation.