Overexpression of protein kinase C-beta1 isoenzyme suppresses SC-236-induced apoptosis in gastric cancer cells

2001 ◽  
Vol 120 (5) ◽  
pp. A664-A665 ◽  
Author(s):  
X JIANG ◽  
S LAM ◽  
H KUNG ◽  
M LIN ◽  
A KOKI ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Kinase C ◽  
Induced Apoptosis

Overexpression of protein kinase C-beta1 isoenzyme suppresses SC-236-induced apoptosis in gastric cancer cells

2001 ◽  
Vol 120 (5) ◽  
pp. A664-A665 ◽  
Author(s):  
Xiaohua Jiang ◽  
S.K. Lam ◽  
H.F. Kung ◽  
Marie C.M. Lin ◽  
Alane T. Koki ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Kinase C ◽  
Induced Apoptosis

Potentiation of Apoptosis by Treatment With the Protein Kinase C-Specific Inhibitor Safingol in Mitomycin C-Treated Gastric Cancer Cells

1995 ◽  
Vol 87 (18) ◽  
pp. 1394-1399 ◽  
Author(s):  
G. K. Schwartz ◽  
A. Haimovitz-Friedman ◽  
S. K. Dhupar ◽  
D. Ehleiter ◽  
P. Maslak ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Mitomycin C ◽  
Specific Inhibitor ◽  
Gastric Cancer Cells ◽  
Kinase C

scholarly journals Protein kinase C β inhibits autophagy and sensitizes cervical cancer Hela cells to cisplatin

2017 ◽  
Vol 37 (2) ◽  
Author(s):  
Na Li ◽  
Wei Zhang
Keyword(s):  
Cervical Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Hela Cells ◽  
B Cell Lymphoma ◽  
Kinase C ◽  
Cervical Cancer Cells ◽  
Pkc Β ◽  
Induced Apoptosis

Recently, autophagy has been indicated to play an essential role in various biological events, such as the response of cervical cancer cells to chemotherapy. However, the exact signalling mechanism that regulates autophagy during chemotherapy remains unclear. In the present study, we investigated the regulation by cisplatin on protein kinase C β (PKC β), on B-cell lymphoma 2 (Bcl-2) and on apoptosis in cervical cancer Hela cells. And then we examined the regulation by cisplatin on autophagy and the role of autophagy on the chemotherapy in Hela cells. In addition, the regulation of the PKC β on the autophagy was also investigated. Our results indicated that cisplatin promoted PKC β in Hela cells. The PKC β inhibitor reduced the cisplatin-induced apoptosis, whereas increased the cisplatin-induced autophagy in Hela cells. On the other side, the PKC β overexpression aggravated the cisplatin-induced apoptosis, whereas down-regulated the cisplatin-induced autophagy. Taken together, our study firstly recognized the involvement of PKC β in the cytotoxicity of cisplatin via inhibiting autophagy in cervical cancer cells. We propose that PKC β would sensitize cervical cancer cells to chemotherapy via reducing the chemotherapy induced autophagy in cancer cells.

Depletion of death-associated protein-3 induces chemoresistance in gastric cancer cells through the β-catenin/LGR5/Bcl-2 axis

2019 ◽  
Vol 67 (5) ◽  
pp. 856-861 ◽  
Author(s):  
Yongning Jia ◽  
Ziyu Li ◽  
Xiaojing Cheng ◽  
Xiaojiang Wu ◽  
Fei Pang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Ectopic Expression ◽  
Nuclear Accumulation ◽  
Apoptosis Resistance ◽  
Gastric Cancer Cells ◽  
Downstream Target ◽  
Novel Strategy ◽  
Induced Apoptosis

Previously, we demonstrated that death-associated protein-3 (DAP3) loss drives chemoresistance in gastric cancer cells. In the present study, we aimed to determine the underlying molecular mechanism. The effect of DAP3 silencing on β-catenin signaling was assessed. The direct mediator of DAP3 silencing-induced chemoresistance was identified. Depletion of DAP3 stimulates nuclear accumulation of β-catenin and enhances β-catenin-dependent transcriptional activity in gastric cancer cells. However, the protein kinase B , , extracellular regulated protein kinase and signal transducer and activator of transcription 3 signaling pathways remain unaffected by DAP3 loss. We found that the downstream target gene LGR5 (leucine-rich G-protein coupled receptor 5) is upregulated in DAP3-depleted gastric cancer cells. Moreover, knockdown of LGR5 resensitizes DAP3-depleted gastric cancer cells to 5-fluorouracil (5-FU) and oxaliplatin. We also observed that ectopic expression of LGR5 reduces apoptosis in gastric cancer cells on treatment with 5-FU and oxaliplatin, which is accompanied by prevention of caspase-3 cleavage. The antiapoptotic protein Bcl-2 is identified as a key mediator of LGR5-induced apoptosis resistance in gastric cancer cells. The present findings indicate that DAP3 deficiency-induced chemoresistance in gastric cancer is at least partially mediated through the β-catenin/LGR5/Bcl-2 axis. Targeting LGR5 may provide a novel strategy to overcome chemoresistance in DAP3-deficient gastric cancer cells.

scholarly journals Involvement of Protein Kinase C δ (PKCδ) in Phorbol Ester-induced Apoptosis in LNCaP Prostate Cancer Cells

2000 ◽  
Vol 275 (11) ◽  
pp. 7574-7582 ◽  
Author(s):  
Teruhiko Fujii ◽  
Marı́a Laura Garcı́a-Bermejo ◽  
Juan Lucas Bernabó ◽  
Jorge Caamaño ◽  
Motoi Ohba ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Phorbol Ester ◽  
Prostate Cancer Cells ◽  
Kinase C ◽  
Induced Apoptosis
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