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Tetrandrine and cancer - An overview on the molecular approach.

Abstract
Tetrandrine has been known in the treatment of tuberculosis, hyperglycemia, negative ionotropic and chronotropic effects on myocardium, malaria, cancer and fever since years together. It has been known that, tetrandrine could modulate multiple signaling molecules such as kinases of cell cycle and rat sarcoma (RAS) pathway along with proteins of tumor suppressor genes, autophagy related, β-catenins, caspases, and death receptors. Moreover, tetrandrine exhibited reversal of drug resistance by modulating P-glyco protein (P-gp) expression levels in different cancers which is an added advantage of this compound compared to other chemotherapy drugs. Though, bioavailability of tetrandrine is a limiting factor, the anticancer activity was observed in animal models without changing any pharmacokinetic parameters. In the present review, role of tetrandrine as kinase inhibitor, inducer of autophagy and caspase pathways and suppressor of RAS mediated cell proliferation were discussed along with inhibition of angiogenesis. It has also been discussed that how tetrandrine potentiate anticancer effect in different types of cancers by modulating multidrug resistance under in vitro and in vivo trials including the available literature on the clinical trials.
AuthorsBhagya N, Chandrashekar K R
JournalBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie (Biomed Pharmacother) Vol. 97 Pg. 624-632 (Jan 2018) ISSN: 1950-6007 [Electronic] France
PMID29101806 (Publication Type: Journal Article, Review)
CopyrightCopyright © 2017 Elsevier Masson SAS. All rights reserved.
Chemical References
  • Antineoplastic Agents, Phytogenic
  • Benzylisoquinolines
  • tetrandrine
Topics
  • Animals
  • Antineoplastic Agents, Phytogenic (chemistry, pharmacology, therapeutic use)
  • Autophagy (drug effects, physiology)
  • Benzylisoquinolines (chemistry, pharmacology, therapeutic use)
  • Cell Line, Tumor
  • Clinical Trials as Topic (methods)
  • Drug Resistance, Multiple (drug effects, physiology)
  • Drug Resistance, Neoplasm (drug effects, physiology)
  • Humans
  • Neoplasms (drug therapy, metabolism)
  • Signal Transduction (drug effects, physiology)

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