Clofibric Acid, a Peroxisome Proliferator-activated Receptor Alpha Ligand, Enhances a Suppressive Effect of Cis-diaminedichloroplatinum on Proliferation of Ovarian Carcinoma Cells

The purpose of this study was to elucidate the possible mechanism that clofibric acid (CA), a peroxisome proliferator-activated receptor α ligand, enhances a suppressive effect of cis-diaminedichloroplatinum (CDDP) on proliferation of the ovarian carcinoma line OVCAR-3. These cells was incubated with 0.5 μM/ml CDDP in the presence or absence of 50 μM CA or incubated with 50 μM CA alone for 72 hr. While treatment with CA alone did not affect proliferation of OVCAR-3 cells, simultaneous treatment with CDDP and CA significantly suppressed proliferation of the cells and significantly induced apoptosis compared to that with CDDP alone. Treatment with CDDP and CA significantly decreased the prostaglandin (PG) E2 level in the medium of the cells compared with treatment with CDDP alone. These results suggest the ability of CA to enhance a suppressive effect of CDDP on proliferation of the ovarian carcinoma cells through reduction of PGE2 level.

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Activation and Expression of Peroxisome Proliferator-Activated Receptor Alpha Are Associated with Tumorigenesis in Colorectal Carcinoma

PPAR Research ◽

10.1155/2019/7486727 ◽

2019 ◽

Vol 2019 ◽

pp. 1-9 ◽

Cited By ~ 3

Author(s):

Tatsuya Morinishi ◽

Yasunori Tokuhara ◽

Hiroyuki Ohsaki ◽

Emi Ibuki ◽

Kyuichi Kadota ◽

...

Keyword(s):

Cell Proliferation ◽

Colorectal Carcinoma ◽

Critical Role ◽

Carcinoma Cells ◽

Peroxisome Proliferator ◽

Normal Epithelium ◽

Peroxisome Proliferator Activated Receptor ◽

Receptor Alpha ◽

Nuclear Expression ◽

Induced Apoptosis

Peroxisome proliferator-activated receptor alpha (PPAR-α) belongs to the PPAR family and plays a critical role in inhibiting cell proliferation and tumorigenesis in various tumors. However, the role of PPAR-αin colorectal tumorigenesis is unclear. In the present study, we found that fenofibrate, a PPAR-αagonist, significantly inhibited cell proliferation and induced apoptosis in colorectal carcinoma cells. In addition, PPAR-αwas expressed in the nucleus of colorectal carcinoma cells, and the expression of nuclear PPAR-αincreased in colorectal carcinoma tissue compared with that of normal epithelium tissue (P<0.01). The correlation between the expression of nuclear PPAR-αand clinicopathological factors was evaluated in human colorectal carcinoma tissues, and the nuclear expression of PPAR-αwas significantly higher in well-to-moderately differentiated adenocarcinoma than in mucinous adenocarcinoma (P<0.05). These findings indicate that activation of PPAR-αmay be involved in anticancer effects in colorectal carcinomas, and nuclear expression of PPAR-αmay be a therapeutic target for colorectal adenocarcinoma treatment.

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

Journal of Cellular Biochemistry ◽

10.1002/jcb.20006 ◽

2004 ◽

Vol 91 (5) ◽

pp. 1043-1052 ◽

Cited By ~ 43

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

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Clofibric acid induces hepatic CYP 2B1/2 via constitutive androstane receptor not via peroxisome proliferator activated receptor alpha in rat

Bioscience Biotechnology and Biochemistry ◽

10.1080/09168451.2014.923302 ◽

2014 ◽

Vol 78 (9) ◽

pp. 1550-1559

Author(s):

Zein Shaban Ibrahim ◽

Mohamed Mohamed Ahmed ◽

Samir Ahmed El-Shazly ◽

Mayumi Ishizuka ◽

Shoichi Fujita

Keyword(s):

Constitutive Androstane Receptor ◽

Clofibric Acid ◽

Peroxisome Proliferator ◽

Peroxisome Proliferator Activated Receptor ◽

Receptor Alpha

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

Clinical Science ◽

10.1042/cs103s302s ◽

2002 ◽

Vol 103 (s2002) ◽

pp. 302S-305S ◽

Cited By ~ 20

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.

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