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Caspase Deficiency: Involvement In Breast Carcinogenesis And Resistance

X. Yang
Published 2001 · Biology

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Abstract : This project was designed to study the incidence and significance of caspase deficiency in breast cancer carcinogenesis and resistance. Task 1 for the first 15 months was to detect caspase expression in breast cancer cell lines and breast cancer tissues. In the past 12 months, we have expanded and cryopreserved 20 cell lines for future study. Detection of caspase expression from breast cancer cell lines revealed that caspase levels varied significantly amongst different cell lines. For example, caspase 6, 8 and 10 levels in HS-578T cells were significantly lower than that of other cell lines. Detection of caspase 3 expression in 40 breast cancer tissues using either immunohistochemistry or Western blot indicated that approximately one fifth of breast cancer tissues had abnormally low or deficient caspase expression. These data suggests that caspase down-regulation/deficiency may have clinical significance, which is consistent with our hypothesis. Caspase detection/screening is currently being continued. Another part of our work was on the characterization of caspase 3 reconstituted MCF-7 cells in response to chemo- and radio- therapies. We found that caspase 3 reconstitution sensitizes MCF-7 cells to both chemo- and radio- therapies. The results have been presented at meeting and a manuscript has been submitted to Cancer Research (under revision).
This paper references
DFF, a Heterodimeric Protein That Functions Downstream of Caspase-3 to Trigger DNA Fragmentation during Apoptosis
X. Liu (1997)
Accumulation of p53 tumor suppressor gene protein: an independent marker of prognosis in breast cancers.
A. Thor (1992)
Apopain/CPP32 cleaves proteins that are essential for cellular repair: a fundamental principle of apoptotic death
L. Casciola-Rosen (1996)
p53-dependent DNA damage-induced apoptosis requires Fas/APO-1-independent activation of CPP32beta.
E. Fuchs (1997)
Caspase-3-generated fragment of gelsolin: effector of morphological change in apoptosis.
S. Kothakota (1997)
Cleavage of sterol regulatory element binding proteins (SREBPs) by CPP32 during apoptosis.
X. Wang (1996)
Bcl-xL is expressed in neuroblastoma cells and modulates chemotherapy-induced apoptosis.
M. Dole (1995)
Cleavage of huntingtin by apopain, a proapoptotic cysteine protease, is modulated by the polyglutamine tract
Y. Goldberg (1996)
The cell-death machine
A. Chinnaiyan (1996)
Cell suicide for beginners
M. Raff (1998)
Distinct Caspase Cascades Are Initiated in Receptor-mediated and Chemical-induced Apoptosis*
X. Sun (1999)
Bax-Dependent Caspase-3 Activation Is a Key Determinant in p53-Induced Apoptosis in Neurons
S. Cregan (1999)
Caspase-3-mediated Cleavage of Protein Kinase C θ in Induction of Apoptosis*
R. Datta (1997)
Cell death: the significance of apoptosis.
A. Wyllie (1980)
D4-GDI, a Substrate of CPP32, Is Proteolyzed during Fas-induced Apoptosis (*)
S. Na (1996)
p53 is involved in but not required for ionizing radiation-induced caspase-3 activation and apoptosis in human lymphoblast cell lines.
Y. Yu (1998)
Apoptosis by Death Factor
S. Nagata (1997)
p53 status affects the rate of the onset but not the overall extent of doxorubicin-induced cell death in rat-1 fibroblasts constitutively expressing c-Myc.
J. Han (1997)
Requirement of the Caspase-3/CPP32 Protease Cascade for Apoptotic Death following Cytokine Deprivation in Hematopoietic Cells*
T. Ohta (1997)
Granzyme B Mimics Apical Caspases
X. Yang (1998)
Essential contribution of caspase 3/CPP32 to apoptosis and its associated nuclear changes.
M. Woo (1998)
Overexpression of the death-promoting gene bax-alpha which is downregulated in breast cancer restores sensitivity to different apoptotic stimuli and reduces tumor growth in SCID mice.
R. Bargou (1996)
Protease activation during apoptosis: Death by a thousand cuts?
S. Martin (1995)
Cell type‐specific inhibition of p53‐mediated apoptosis by mdm2.
Y. Haupt (1996)
A Combinatorial Approach Defines Specificities of Members of the Caspase Family and Granzyme B
N. Thornberry (1997)
Human ICE/CED-3 Protease Nomenclature
E. Alnemri (1996)
Yama/CPP32β, a mammalian homolog of CED-3, is a CrmA-inhibitable protease that cleaves the death substrate poly(ADP-ribose) polymerase
M. Tewari (1995)
Caspases: Intracellular Signaling by Proteolysis
G. Salvesen (1997)
Apoptosis in the pathogenesis and treatment of disease
C. Thompson (1995)
Proteolysis of Fodrin (Non-erythroid Spectrin) during Apoptosis (*)
S. J. Martin (1995)
Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis
D. Nicholson (1995)
Caspase-3 controls both cytoplasmic and nuclear events associated with Fas-mediated apoptosis in vivo.
T. Zheng (1998)
Caspase-14 Is a Novel Developmentally Regulated Protease*
S. Hu (1998)
Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice
K. Kuida (1996)
The tumor suppressor genes.
A. Levine (1993)
Disruption of p53 in human cancer cells alters the responses to therapeutic agents.
F. Bunz (1999)
Caspases: enemies within.
N. Thornberry (1998)
Ceramide synthase mediates daunorubicin-induced apoptosis: An alternative mechanism for generating death signals
R. Bose (1995)
Overexpression of the E2F-1 transcription factor gene mediates cell transformation.
Yang Xh (1995)
Disruption of p53 function sensitizes breast cancer MCF-7 cells to cisplatin and pentoxifylline.
S. Fan (1995)
Caspase-3 activation during apoptosis caused by glutathione–doxorubicin conjugate
T. Asakura (1999)
Advanced mammalian gene transfer: high titre retroviral vectors with multiple drug selection markers and a complementary helper-free packaging cell line.
J. Morgenstern (1990)
p53 status and the efficacy of cancer therapy in vivo.
S. Lowe (1994)
p53 is required for radiation-induced apoptosis in mouse thymocytes
S. Lowe (1993)
Frameshift mutations at mononucleotide repeats in caspase-5 and other target genes in endometrial and gastrointestinal cancer of the microsatellite mutator phenotype.
S. Schwartz (1999)
CPP32, a novel human apoptotic protein with homology to Caenorhabditis elegans cell death protein Ced-3 and mammalian interleukin-1 beta-converting enzyme.
T. Fernandes-Alnemri (1994)
bax-deficiency promotes drug resistance and oncogenic transformation by attenuating p53-dependent apoptosis.
M. McCurrach (1997)
Dose and dose intensity of adjuvant chemotherapy for stage II, node-positive breast carcinoma.
W. Wood (1994)
Specific cleavage of the 70-kDa protein component of the U1 small nuclear ribonucleoprotein is a characteristic biochemical feature of apoptotic cell death.
L. Casciola-Rosen (1994)
p21-induced cycle arrest in G1 protects cells from apoptosis induced by UV-irradiation or RNA polymerase II blockage
N. Bissonnette (1998)
Apoptosis in cancer therapy: Crossing the threshold
D. Fisher (1994)
p53 in growth control and neoplasia.
T. M. Gottlieb (1996)
Farnesyltransferase inhibitors induce cytochrome c release and caspase 3 activation preferentially in transformed cells.
N. Suzuki (1998)
Adriamycin-induced DNA Adducts Inhibit the DNA Interactions of Transcription Factors and RNA Polymerase (*)
S. Cutts (1996)
Caspase-3 Is Required for DNA Fragmentation and Morphological Changes Associated with Apoptosis*
R. Jänicke (1998)
Caspase-mediated cleavage of p21Waf1/Cip1 converts cancer cells from growth arrest to undergoing apoptosis
Y. Zhang (1999)
Expression of bcl-xL can confer a multidrug resistance phenotype.
A. Minn (1995)

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