Abstract
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-α in colorectal tumorigenesis is unclear. In the present study, we found that fenofibrate, a PPAR-α agonist, significantly inhibited cell proliferation and induced apoptosis in colorectal carcinoma cells. In addition, PPAR-α was expressed in the nucleus of colorectal carcinoma cells, and the expression of nuclear PPAR-α increased in colorectal carcinoma tissue compared with that of normal epithelium tissue (P<0.01). The correlation between the expression of nuclear PPAR-α and clinicopathological factors was evaluated in human colorectal carcinoma tissues, and the nuclear expression of PPAR-α was significantly higher in well-to-moderately differentiated adenocarcinoma than in mucinous adenocarcinoma (P<0.05). These findings indicate that activation of PPAR-α may be involved in anticancer effects in colorectal carcinomas, and nuclear expression of PPAR-α may be a therapeutic target for colorectal adenocarcinoma treatment.
Highlights
More than 1.2 million colorectal carcinomas are diagnosed every year, accounting for approximately 10% of all carcinomas worldwide [1]
Expression of peroxisome proliferator-activated receptors (PPARs)-α protein was examined by western blotting in the colorectal carcinoma cell lines, and there was no difference in the amount of PPARα protein in Caco-2 and SW620 cells (Figures 1(b) and 1(c))
We examined the activity of PPAR-α by fenofibrate in colorectal carcinoma cell lines
Summary
More than 1.2 million colorectal carcinomas are diagnosed every year, accounting for approximately 10% of all carcinomas worldwide [1]. There was considerable progress in the diagnosis and treatment of colorectal carcinomas in the past 10 years, but some problems in detecting and managing this disease remain. A deeper understanding of the mechanism of colorectal carcinomas at the molecular level improves early diagnosis, prognostic evaluation, and disease control [2]. The relationship of anticancer effects between colorectal carcinomas and peroxisome proliferator-activated receptors (PPARs) has been reported [3, 4]. PPARs are nuclear hormone receptors and are expressed in various species including humans [5]. PPARγ can modulate the growth and differentiation of colorectal cancer cells [9], and ligand-dependent PPAR-γ activation influences subcellular localization in colorectal carcinoma cell lines [10]. PPAR-α regulates important cellular functions, including cell proliferation, differentiation, energy metabolism, oxidative stress, inflammation, circadian
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