Abstract
Solid cancer remains a major cause of death in the world. As limited treatment options are currently available to patients with solid cancer, novel preventive control and effective therapeutic approaches are considered to be reasonable and decisive measures to combat this disease. The plant-derived triterpenoids, commonly used for medicinal purposes in many Asian countries, poses various pharmacological properties. A large number of triterpenoids exhibit cytotoxicity against a variety of cancer cells, and cancer preventive, as well as anticancer efficacy in preclinical animal models. To improve antitumor activity, some synthetic triterpenoid derivatives have been synthesized, including cyano-3,12-dioxooleana-1,9(11)- dien-28-oic (CDDO), its methyl ester (CDDO-Me), and imidazolide (CDDO-Im) derivatives. In this review, we will critically examine the current preclinical evidences of cancer preventive and therapeutic activity about one of the synthetic triterpenoids, CDDO-Me. Both in vitro and in vivo effects of this agent and related molecular mechanisms are presented.
Highlights
It has become evident that cancer development underlies a collection of multiple genetic abnormalities through a multistep, mutagenic process [1,2]
The complexity of the genetic lesions and the variation of the derivative phenotypic changes of cancer cells indicate that multifunctional drugs capable of affecting cancer cells at various levels must be used for the treatment of these diseases [3,4]
These results suggest that CDDO-Me has the potential to prevent BRCA1-mutated breast cancer
Summary
It has become evident that cancer development underlies a collection of multiple genetic abnormalities through a multistep, mutagenic process [1,2]. In BRCA1-deficient cell lines, the triterpenoids directly interacted with ErbB2, decreased constitutive phosphorylation of ErbB2, inhibited proliferation, and induced G0/G1 arrest These results suggest that CDDO-Me has the potential to prevent BRCA1-mutated breast cancer. Akt: protein kinase B1;Bad: Bcl-2-associated death promoter; Bcl-2:B-cell lymphoma 2; BCL-xL: B-cell lymphoma extra large; c-FLIP: cellular FLICE inhibitory protein; CHOP: CCAAT/enhancer binding protein homologous protein; COX-2: cyclooxygenase 2; DR:death receptor; ER: endoplasmic reticulum; GSH: glutathione; hTERT: human telomerase reverse transcriptase; JNK: c-Jun NH2-terminal kinase; MDR: multidrug resistant; MDSC: myeloid-derived suppressor cells; mTOR :mammalian target of rapamycin; NAC: N-acetylcysteine; NF-κB: nuclear factor-κB; ROS: reactive oxygen species; STAT3: transcription factor signal transducers and activators of transcription 3; TRAIL :TNF related apoptosis inducing ligand; VEGF: vascular endothelial growth factor; XIAP: X-linked inhibitor of apoptosis protein. For the observed objective tumor responses, other synthetic triterpenoids were suggested for continued development in solid cancer treatment
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