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

PPAR Research ◽  
2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
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.

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

2007 ◽  
Vol 1 ◽  
pp. CMO.S283
Author(s):  
Yoshihito Yokoyama ◽  
Bing Xin ◽  
Tatsuhiko Shigeto ◽  
Masayuki Futagami ◽  
Hideki Mizunuma
Keyword(s):  
Ovarian Carcinoma ◽  
Suppressive Effect ◽  
Clofibric Acid ◽  
Carcinoma Cells ◽  
Peroxisome Proliferator ◽  
Simultaneous Treatment ◽  
Peroxisome Proliferator Activated Receptor ◽  
Receptor Alpha ◽  
Ovarian Carcinoma Cells ◽  
Induced Apoptosis

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.

scholarly journals Differential Effects of Estrogen Receptor Alpha and Beta on Endogenous Ligands of Peroxisome Proliferator-Activated Receptor Gamma in Papillary Thyroid Cancer

2021 ◽  
Vol 12 ◽  
Author(s):  
Shucai Yang ◽  
Zhongqin Gong ◽  
Zhimin Liu ◽  
Minghui Wei ◽  
Lingbin Xue ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Papillary Thyroid Cancer ◽  
Estrogen Receptor Alpha ◽  
Peroxisome Proliferator ◽  
Papillary Thyroid ◽  
Peroxisome Proliferator Activated Receptor ◽  
Receptor Alpha ◽  
Induced Apoptosis

PurposeThe inhibition of estrogen receptor alpha (ERα) or the activation of ERβ can inhibit papillary thyroid cancer (PTC), but the precise mechanism is not known. We aimed to explore the role of ERα and ERβ on the production of endogenous peroxisome proliferator-activated receptor gamma (PPARγ) ligands in PTC.Methods2 PTC cell lines, 32 pairs of PTC tissues and matched normal thyroid tissues were used in this study. The levels of endogenous PPARγ ligands 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE), 13-S-hydroxyoctadecadienoic acid (13(S)-HODE), and15-deoxy-Δ12,14-prostaglandin J2 (PGJ2) were measured by ELISA.ResultsThe levels of PGJ2 and 15(S)-HETE were significantly reduced in PTC, but 13(S)-HODE was not changed. Activation of ERα or inhibition of ERβ significantly downregulated the production of PGJ2, 15(S)-HETE and 13(S)-HODE, whereas inhibition of ERα or activation of ERβ markedly upregulated the production of these three ligands. Application of endogenous PPARγ ligands inhibited growth, induced apoptosis of cancer cells, and promoted the efficacy of chemotherapy.ConclusionThe levels of endogenous PPARγ ligands PGJ2 and 15(S)-HETE are significantly decreased in PTC. The inhibition of ERα or activation of ERβ can inhibit PTC by stimulating the production of endogenous PPARγ ligands to induce apoptosis in cancer cells.

scholarly journals Chondrosarcoma and Peroxisome Proliferator-Activated Receptor

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-7 ◽  
Author(s):  
K. Nishida ◽  
T. Kunisada ◽  
Z. N. Shen ◽  
Y. Kadota ◽  
K. Hashizume ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Malignant Tumors ◽  
Peroxisome Proliferator ◽  
Dependent Manner ◽  
Cytochrome C Release ◽  
Peroxisome Proliferator Activated Receptor ◽  
Human Chondrosarcoma ◽  
Induced Apoptosis ◽  
Ppar Ligands

Induction of differentiation and apoptosis in cancer cells by ligands of PPAR is a novel therapeutic approach to malignant tumors. Chondrosarcoma (malignant cartilage tumor) and OUMS-27 cells (cell line established from grade III human chondrosarcoma) express PPAR. PPAR ligands inhibited cell proliferation in a dose-dependent manner, and induced apoptosis of OUMS-27. The higher-grade chondrosarcoma expressed a higher amount of antiapoptotic Bcl-xL in vivo. The treatment of OUMS-27 by 15d-PG, the most potent endogenous ligand for PPAR, downregulated expression of Bcl-xL and induced transient upregulation of proapoptotic Bax, which could accelerate cytochrome c release from mitochondria to the cytosol, followed by induction of caspase-dependent apoptosis. 15d-PG induced the expression of CDK inhibitor p21 protein in human chondrosarcoma cells, which appears to be involved in the mechanism of inhibition of cell proliferation. These findings suggest that targeted therapy with PPAR ligands could be a novel strategy against chondrosarcoma.

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