scholarly journals Drug-induced caspase 8 upregulation sensitises cisplatin-resistant ovarian carcinoma cells to rhTRAIL-induced apoptosis

2011 ◽  
Vol 104 (8) ◽  
pp. 1278-1287 ◽  
Author(s):  
E W Duiker ◽  
A Meijer ◽  
A R M van der Bilt ◽  
G J Meersma ◽  
N Kooi ◽  
...  
Keyword(s):  
Ovarian Carcinoma ◽  
Carcinoma Cells ◽  
Caspase 8 ◽  
Drug Induced ◽  
Ovarian Carcinoma Cells ◽  
Induced Apoptosis

Mechanism of taxol-induced apoptosis in human SKOV3 ovarian carcinoma cells

2004 ◽  
Vol 91 (5) ◽  
pp. 1043-1052 ◽  
Author(s):  
Hak Jun Ahn ◽  
Yeong Shik Kim ◽  
Joung-Uk Kim ◽  
Sung Min Han ◽  
Jin Woo Shin ◽  
...  
Keyword(s):  
Ovarian Carcinoma ◽  
Carcinoma Cells ◽  
Ovarian Carcinoma Cells ◽  
Induced Apoptosis

Endothelin-1 acts as a survival factor in ovarian carcinoma cells

2002 ◽  
Vol 103 (s2002) ◽  
pp. 302S-305S ◽  
Author(s):  
Donatella DEL BUFALO ◽  
Valeriana DI CASTRO ◽  
Annamaria BIROCCIO ◽  
Debora SALANI ◽  
Laura ROSANÒ ◽  
...  
Keyword(s):  
Ovarian Carcinoma ◽  
Cell Lines ◽  
Carcinoma Cells ◽  
Ovarian Carcinomas ◽  
Endothelin 1 ◽  
Carcinoma Cell Lines ◽  
Ovarian Carcinoma Cells ◽  
Novel Approach ◽  
Eta Receptor ◽  
Induced Apoptosis

The aim of this study was to evaluate the role of endothelin-1 (ET-1) in the sensitivity of ovarian carcinoma to paclitaxel, one of the most common drugs used for the management of this tumour histotype. ET-1 is a powerful mitogenic peptide produced by ovarian carcinomas and it acts as an autocrine growth factor, selectively through ETA receptor (ETAR), which is predominantly expressed in this tumour. OVCA 433 and HEY, two ovarian carcinoma cell lines, which produce elevated amounts of ET-1 and express abundantly high-affinity ETARs, were used. As demonstrated by sub-G1 peak in DNA content histograms and terminal transferase deoxytidyl uridine end labelling assay, we found that paclitaxel induces cytotoxic effect through the activation of apoptosis in both cell lines. When the treatment with paclitaxel was performed in association with ET-1, paclitaxel-induced apoptosis was inhibited. In order to evaluate which ET-1 receptor mediated the effect of ET-1 on protection from paclitaxel-induced apoptosis, we performed experiments using two selective antagonists for ETAR (BQ-123) and for ETBR (BQ-788). We showed that ETAR blockade inhibits the ET-1-induced survival activity against paclitaxel-mediated apoptosis. However, no effect was observed on blocking ETBR with BQ-788. Our results establish a novel role for ET-1 in determining survival of ovarian carcinoma cells and suggest that pharmacological ETAR blockade using a specific ETAR antagonist may provide a novel approach to the treatment of ovarian carcinoma in combination therapy.

Cysteine-rich 61 (CYR61) inhibits cisplatin-induced apoptosis in ovarian carcinoma cells

2008 ◽  
Vol 31 (1) ◽  
pp. 23-28 ◽  
Author(s):  
Seung Bae Rho ◽  
Hyun-Jung Byun ◽  
Sang-Yoon Park ◽  
Taehoon Chun
Keyword(s):  
Ovarian Carcinoma ◽  
Carcinoma Cells ◽  
Ovarian Carcinoma Cells ◽  
Induced Apoptosis

scholarly journals Cysteine-rich 61 (CYR61) inhibits cisplatin-induced apoptosis in ovarian carcinoma cells

2008 ◽  
Vol 31 (1) ◽  
pp. 29-29
Author(s):  
Seung Bae Rho ◽  
Jong Soo Woo ◽  
Taehoon Chun ◽  
Sang-Yoon Park
Keyword(s):  
Ovarian Carcinoma ◽  
Carcinoma Cells ◽  
Ovarian Carcinoma Cells ◽  
Induced Apoptosis

Cooperation between p53 and p73 in cisplatin-induced apoptosis in ovarian carcinoma cells

2008 ◽  
Vol 263 (1) ◽  
pp. 140-144 ◽  
Author(s):  
Sabina Carla Righetti ◽  
Paola Perego ◽  
Nives Carenini ◽  
Franco Zunino
Keyword(s):  
Ovarian Carcinoma ◽  
Carcinoma Cells ◽  
Ovarian Carcinoma Cells ◽  
Induced Apoptosis

scholarly journals Molecular mechanism of phenoxodiol-induced apoptosis in ovarian carcinoma cells

Cancer ◽  
2006 ◽  
Vol 106 (3) ◽  
pp. 599-608 ◽  
Author(s):  
Ayesha B. Alvero ◽  
David O'Malley ◽  
David Brown ◽  
Graham Kelly ◽  
Manish Garg ◽  
...  
Keyword(s):  
Ovarian Carcinoma ◽  
Molecular Mechanism ◽  
Carcinoma Cells ◽  
Ovarian Carcinoma Cells ◽  
Induced Apoptosis
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