Verrucarin A, a protein synthesis inhibitor, induces growth inhibition and apoptosis in breast cancer cell lines MDA-MB-231 and T47D

Verrucarin A (VA), a protein synthesis inhibitor, derived from the pathogen fungus Myrothecium verrucaria, inhibits growth of leukemia cell lines and activates caspases and apoptosis and inflammatory signaling in macrophages. We have investigated VA-induced growth inhibition in breast cancer cells M...

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Bibliographic Details
Published in:Biotechnology letters 2013-09, Vol.35 (9), p.1395-1403
Main Authors: Palanivel, Kandasamy, Kanimozhi, Veerasamy, Kadalmani, Balamuthu, Akbarsha, Mohammad Abdulkader
Format: Article
Language:English
Subjects:
Activation
Antineoplastic Agents - isolation & purification
Antineoplastic Agents - pharmacology
Apoptosis
Applied Microbiology
Biochemistry
Biomedical and Life Sciences
Biomedical research
Biotechnology
Breast
Breast cancer
breast neoplasms
Cancer
caspase-3
Cell Line, Tumor
Cell Proliferation - drug effects
chromatin
Female
fungi
Humans
Hypocreales - chemistry
Immunologic Factors - isolation & purification
Immunologic Factors - pharmacology
Inhibition
Inhibitor drugs
Inhibitors
Leukemia
Life Sciences
macrophages
Macrophages - drug effects
Microbiology
Myrothecium verrucaria
Natural products
Original Research Paper
pathogens
Protein synthesis
Protein Synthesis Inhibitors - isolation & purification
Protein Synthesis Inhibitors - pharmacology
shrinkage
Trichothecenes - isolation & purification
Trichothecenes - pharmacology
viability
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Summary:Verrucarin A (VA), a protein synthesis inhibitor, derived from the pathogen fungus Myrothecium verrucaria, inhibits growth of leukemia cell lines and activates caspases and apoptosis and inflammatory signaling in macrophages. We have investigated VA-induced growth inhibition in breast cancer cells MDA-MB-231 and T47D and, particularly, the mechanism of VA-induced apoptosis. VA treatment brought about apoptotic cell death in a dose- and time-dependent manner which was associated with chromatin condensation, cell shrinkage, nuclear fragmentation and intracellular ROS production. Mitochondrial membrane depolarization, activation of caspase-3, down-regulation of Bcl-2 expression and up-regulation of Bax and p53 expression were observed. VA thus affects the viability of both the breast cancer cells by triggering ROS-mediated intrinsic mechanism of apoptosis.
ISSN:0141-5492
1573-6776
DOI:10.1007/s10529-013-1238-y