Synthetic triterpenoids inhibit growth and induce apoptosis in human glioblastoma and neuroblastoma cells through inhibition of prosurvival Akt, NF-kappaB and Notch1 signaling.
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Preclinical evidences toward the use of triterpenoid CDDO-Me for solid cancer prevention and treatmentCell Proliferation in NeuroblastomaSynthetic triterpenoids target the Arp2/3 complex and inhibit branched actin polymerization.Oleanolic acid suppresses migration and invasion of malignant glioma cells by inactivating MAPK/ERK signaling pathwayNatural triterpenic diols promote apoptosis in astrocytoma cells through ROS-mediated mitochondrial depolarization and JNK activationOleanane triterpenoid CDDO-Me inhibits growth and induces apoptosis in prostate cancer cells through a ROS-dependent mechanism.Screening a panel of drugs with diverse mechanisms of action yields potential therapeutic agents against neuroblastoma.Nuclear factor kappaB inhibitors alleviate and the proteasome inhibitor PS-341 exacerbates radiation toxicity in zebrafish embryosPPAR-γ ligands repress TGFβ-induced myofibroblast differentiation by targeting the PI3K/Akt pathway: implications for therapy of fibrosis.The triterpenoid CDDO-Me delays murine acute graft-versus-host disease with the preservation of graft-versus-tumor effects after allogeneic bone marrow transplantation.Induction of Apoptosis in Pancreatic Cancer Cells by CDDO-Me Involves Repression of Telomerase through Epigenetic Pathways.The functional role of Notch signaling in human gliomas.The triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic-acid methyl ester has potent anti-diabetic effects in diet-induced diabetic mice and Lepr(db/db) miceBardoxolone methyl (CDDO-Me) as a therapeutic agent: an update on its pharmacokinetic and pharmacodynamic properties.A novel anticancer therapy that simultaneously targets aberrant p53 and Notch activities in tumorsSynthetic triterpenoid CDDO prevents the progression and metastasis of prostate cancer in TRAMP mice by inhibiting survival signaling.CDDO-Me: A Novel Synthetic Triterpenoid for the Treatment of Pancreatic CancerPrevention of Prostate Cancer with Oleanane Synthetic Triterpenoid CDDO-Me in the TRAMP Mouse Model of Prostate CancerOleanane triterpenoid CDDO-Me inhibits Akt activity without affecting PDK1 kinase or PP2A phosphatase activity in cancer cells.Synthetic oleanane triterpenoids: multifunctional drugs with a broad range of applications for prevention and treatment of chronic disease.CDDO-Me inhibits tumor growth and prevents recurrence of pancreatic ductal adenocarcinomaThe triterpenoid CDDO-Me promotes hematopoietic progenitor expansion and myelopoiesis in mice.Inhibition of cell proliferation and induction of apoptosis by oleanane triterpenoid (CDDO-Me) in pancreatic cancer cells is associated with the suppression of hTERT gene expression and its telomerase activityTelomerase reverse transcriptase (TERT) is a therapeutic target of oleanane triterpenoid CDDO-Me in prostate cancerInhibition of telomerase activity by oleanane triterpenoid CDDO-Me in pancreatic cancer cells is ROS-dependent.Cell survival signaling in neuroblastoma.ROS mediate proapoptotic and antisurvival activity of oleanane triterpenoid CDDO-Me in ovarian cancer cellsSynthetic oleanane triterpenoid, CDDO-Me, induces apoptosis in ovarian cancer cells by inhibiting prosurvival AKT/NF-κB/mTOR signaling.Role of reactive oxygen species (ROS) in CDDO-Me-mediated growth inhibition and apoptosis in colorectal cancer cells.Synthetic triterpenoids inhibit growth, induce apoptosis and suppress pro-survival Akt, mTOR and NF-{kappa}B signaling proteins in colorectal cancer cellsHuman neuroblastoma cells rapidly enter cell cycle arrest and apoptosis following exposure to C-28 derivatives of the synthetic triterpenoid CDDO.Inhibition of cell proliferation and induction of apoptosis by CDDO-Me in pancreatic cancer cells is ROS-dependent.Oleanane triterpenoid CDDO-Me inhibits growth and induces apoptosis in prostate cancer cells by independently targeting pro-survival Akt and mTORCDDO-imidazolide mediated inhibition of malignant cell growth in Waldenström macroglobulinemiaIdentification of unique sensitizing targets for anti-inflammatory CDDO-Me in metastatic melanoma by a large-scale synthetic lethal RNAi screening.Oleanolic acid and its synthetic derivatives for the prevention and therapy of cancer: preclinical and clinical evidence.Current evidence on the anticancer potential of Chios mastic gum.Nuclear factor-κB in glioblastoma: insights into regulators and targeted therapy.A new development of triterpene acid-containing extracts from Viscum album L. displays synergistic induction of apoptosis in acute lymphoblastic leukaemia.Synthetic triterpenoid cyano enone of methyl boswellate activates intrinsic, extrinsic, and endoplasmic reticulum stress cell death pathways in tumor cell lines.
P2860
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P2860
Synthetic triterpenoids inhibit growth and induce apoptosis in human glioblastoma and neuroblastoma cells through inhibition of prosurvival Akt, NF-kappaB and Notch1 signaling.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
Synthetic triterpenoids inhibi ...... F-kappaB and Notch1 signaling.
@en
type
label
Synthetic triterpenoids inhibi ...... F-kappaB and Notch1 signaling.
@en
prefLabel
Synthetic triterpenoids inhibi ...... F-kappaB and Notch1 signaling.
@en
P2093
P1476
Synthetic triterpenoids inhibi ...... F-kappaB and Notch1 signaling.
@en
P2093
Dorrah Deeb
Scott A Dulchavsky
Subhash C Gautam
Xiaohua Gao
Yongbo Liu
P2860
P2888
P304
P356
10.1007/S11060-007-9364-9
P577
2007-03-15T00:00:00Z
P6179
1013831459