Document Detail


Mu-calpain activation in beta-lapachone-mediated apoptosis.
MedLine Citation:
PMID:  12750552     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Beta-lapachone (beta-Lap) triggers apoptosis in a number of human breast and prostate cancer cell lines through a unique apoptotic pathway that is dependent upon NQO1, a two-electron reductase. Recently, our laboratory showed that beta-lap-exposed MCF-7 cells exhibited an early increase in intracellular cytosolic Ca(2+) from endoplasmic reticulum stores, and that BAPTA-AM (an intracellular Ca(2+) chelator) blocked these early increases and partially inhibited all aspects of beta-lap-induced apoptosis. We now show that exposure of NQO1-expressing breast cancer cells to beta-lap stimulates a unique proteolytic apoptotic pathway involving mu-calpain activation. No apparent activation of m-calpain was noted. Upon activation, mu-calpain translocated to the nucleus concomitant with specific nuclear proteolytic events. Apoptotic responses in beta-lap-exposed NQO1-expressing cells were significantly delayed and survival enhanced by exogenous over-expression of calpastatin, a natural inhibitor of mu- and m-calpains. Furthermore, purified mu-calpain cleaved PARP to a unique fragment (approximately 60 kDa), not previously reported for calpains. We provide evidence that beta-lap-induced, mu-calpain-stimulated apoptosis does not involve any known apoptotic caspases; the activated fragments of caspases were not observed after beta-lap exposures, nor were there any changes in the pro-enzyme forms as measured by Western blot analyses. The ability of beta-lap to trigger an apparently novel, p53-independent, calpain-mediated apoptotic cell death further support the development of this drug for improved breast cancer therapy.
Authors:
Colleen Tagliarino; John J Pink; Kathryn E Reinicke; Sara M Simmers; Shelly M Wuerzberger-Davis; David A Boothman
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Cancer biology & therapy     Volume:  2     ISSN:  1538-4047     ISO Abbreviation:  Cancer Biol. Ther.     Publication Date:    2003 Mar-Apr
Date Detail:
Created Date:  2003-05-16     Completed Date:  2003-10-16     Revised Date:  2012-05-28    
Medline Journal Info:
Nlm Unique ID:  101137842     Medline TA:  Cancer Biol Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  141-52     Citation Subset:  IM    
Affiliation:
Departments of Radiation Oncology and Pharmacology,Case Western Reserve University, Cleveland, Ohio 44106-4942, USA.
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MeSH Terms
Descriptor/Qualifier:
Antibiotics, Antineoplastic / pharmacology*
Apoptosis / drug effects*
Blotting, Western
Breast Neoplasms / drug therapy,  metabolism*,  pathology*
Calcium / metabolism
Calcium-Binding Proteins / pharmacology
Calpain / antagonists & inhibitors,  metabolism*
Caspases / metabolism
Cell Nucleus / metabolism
Colony-Forming Units Assay
Cysteine Proteinase Inhibitors / pharmacology
Cytosol / metabolism
Enzyme Activation
Female
Humans
In Situ Nick-End Labeling
Microscopy, Confocal
NAD(P)H Dehydrogenase (Quinone) / genetics,  metabolism,  pharmacology*
Naphthoquinones / pharmacology*
Poly(ADP-ribose) Polymerases / metabolism
Protein Transport
Tumor Cells, Cultured
Tumor Suppressor Protein p53 / metabolism
Chemical
Reg. No./Substance:
0/Antibiotics, Antineoplastic; 0/Calcium-Binding Proteins; 0/Cysteine Proteinase Inhibitors; 0/Naphthoquinones; 0/Tumor Suppressor Protein p53; 4707-32-8/beta-lapachone; 7440-70-2/Calcium; 79079-11-1/calpastatin; EC 1.6.5.2/NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2/NQO1 protein, human; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 3.4.22.-/Calpain; EC 3.4.22.-/Caspases; EC 3.4.22.-/m-calpain; EC 3.4.22.-/mu-calpain
Comments/Corrections
Comment In:
Cancer Biol Ther. 2003 Mar-Apr;2(2):153-4   [PMID:  12750553 ]

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