scholarly journals Protein kinase Cδ and caspase-3 modulate TRAIL-induced apoptosis in breast tumor cells

2010 ◽  
Vol 111 (4) ◽  
pp. 979-987 ◽  
Author(s):  
Shuping Yin ◽  
Seema Sethi ◽  
Kaladhar B. Reddy
Keyword(s):  
Protein Kinase ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Caspase 3 ◽  
Breast Tumor Cells ◽  
Induced Apoptosis ◽  
Protein Kinase Cδ

Focal Adhesion Kinase and Protein Kinase B Cooperate to Suppress Doxorubicin-Induced Apoptosis of Breast Tumor Cells

2006 ◽  
Vol 70 (4) ◽  
pp. 1330-1339 ◽  
Author(s):  
Maroesja J. van Nimwegen ◽  
Merei Huigsloot ◽  
Annamarie Camier ◽  
Ine B. Tijdens ◽  
Bob van de Water
Keyword(s):  
Protein Kinase ◽  
Focal Adhesion Kinase ◽  
Tumor Cells ◽  
Focal Adhesion ◽  
Breast Tumor ◽  
Protein Kinase B ◽  
Breast Tumor Cells ◽  
Induced Apoptosis

Expression of HIF-1α ODD domain fused canine caspase 3 by EGFR promoter-driven adenovirus vector induces cytotoxicity in canine breast tumor cells under hypoxia

2016 ◽  
Vol 40 (3-4) ◽  
pp. 131-139 ◽  
Author(s):  
Mariko Okamoto ◽  
Ai Asamura ◽  
Ko Tanaka ◽  
Takefumi Soeda ◽  
Kyo Watanabe ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Breast Tumor ◽  
Caspase 3 ◽  
Adenovirus Vector ◽  
Breast Tumor Cells

Nanomolar concentration of NSC606985, a camptothecin analog, induces leukemic-cell apoptosis through protein kinase Cδ–dependent mechanisms

Blood ◽  
2005 ◽  
Vol 105 (9) ◽  
pp. 3714-3721 ◽  
Author(s):  
Man-Gen Song ◽  
Shen-Meng Gao ◽  
Ke-Ming Du ◽  
Min Xu ◽  
Yun Yu ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Caspase 3 ◽  
Specific Inhibitor ◽  
Leukemic Cell ◽  
K562 Cells ◽  
Early Event ◽  
Apoptosis Induction ◽  
Proteolytic Activation ◽  
Induced Apoptosis ◽  
Protein Kinase Cδ

AbstractAs a promising new class of anticancer drugs, camptothecins have advanced to the forefront of several areas of therapeutic and developmental chemotherapy. In the present study, we report that NSC606985, a rarely studied camptothecin analog, induces apoptosis in acute myeloid leukemia (AML) cells NB4 and U937 and inhibits the proliferation without cell death in breakpoint cluster region–Abelson murine leukemia (bcr-abl) kinase-carrying leukemic K562 cells. For apoptosis induction or growth arrest, nanomolar concentrations of NSC606985 are sufficient. At such low concentrations, this agent also significantly inhibits the clonogenic activity of hematopoietic progenitors from patients with AML. For apoptosis induction, NSC606985 rapidly induces the proteolytic activation of protein kinase Cδ (PKCδ) with loss of mitochondrial transmembrane potential (ΔΨm) and caspase-3 activation. Cotreatment with rottlerin, a PKCδ-specific inhibitor, completely blocks NSC606985-induced mitochondrial ΔΨm loss and caspase-3 activation, while the inhibition of caspase-3 by z-DEVD-fluoromethyl ketone (Z-DEVD-fmk) only partially attenuates PKCδ activation and apoptosis. These data indicate that NSC606985-induced PKCδ activation is an early event upstream to mitochondrial ΔΨm loss and caspase-3 activation, while activated caspase-3 has an amplifying effect on PKCδ proteolysis. In addition, NSC606985-induced apoptosis by PKCδ also involves caspase-3–independent mechanisms. Taken together, our results suggest that NSC606985 is a potential agent for the treatment of AML.

scholarly journals Two Faces of Protein Kinase Cδ: The Contrasting Roles of PKCδ in Cell Survival and Cell Death

2010 ◽  
Vol 10 ◽  
pp. 2272-2284 ◽  
Author(s):  
Alakananda Basu ◽  
Deepanwita Pal
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Cell Survival ◽  
Caspase 3 ◽  
Critical Role ◽  
Tumor Promotion ◽  
Cellular Processes ◽  
Proapoptotic Protein ◽  
Induced Apoptosis ◽  
Protein Kinase Cδ

Protein kinase Cδ (PKCδ) is a member of the PKC family that plays a critical role in the regulation of various cellular processes, including cell proliferation, cell death, and tumor promotion. Since the identification that PKCδ is a substrate for caspase-3, there has been overwhelming literature that linked PKCδ with proapoptotic signaling. While PKCδ generally functions as a proapoptotic protein during DNA damage-induced apoptosis, it can act as an antiapoptotic protein during receptor-initiated cell death. PKCδ has also been implicated in tumor suppression as well as survival of several cancers. The function of PKCδ depends on various factors, including its localization, tyrosine phosphorylation, and the presence of other pro- and antiapoptoic signaling molecules. This review discusses the current literature on the contrasting roles of PKCδ in cell survival and cell death.

scholarly journals 6-Hydroxydopamine-induced Apoptosis Is Mediated via Extracellular Auto-oxidation and Caspase 3-dependent Activation of Protein Kinase Cδ

2005 ◽  
Vol 281 (9) ◽  
pp. 5373-5382 ◽  
Author(s):  
Katharine Hanrott ◽  
Louise Gudmunsen ◽  
Michael J. O'Neill ◽  
Susan Wonnacott
Keyword(s):  
Protein Kinase ◽  
Caspase 3 ◽  
Induced Apoptosis ◽  
6 Hydroxydopamine ◽  
Protein Kinase Cδ
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