PPARgamma inhibitors also reduced CRC cell migration and invasion in assays in vitro and reduced both the number and size of metastases in a HT-29/SCID xenograft metastatic model of CRC.
Here, we analyzed a series of chiral phenoxyacetic acid analogues for their ability to inhibit colorectal cancer (CRC) cells growth by binding PPARγ as partial agonists as assessed in transactivation assays of a PPARG-reporter gene.
Here, we provide the first evidence that elevated PPARδ expression and/or activation of PPARδ antagonize the ability of PPARγ to induce colorectal carcinoma cell death.
Since higher levels of miR-130b are found in advanced tumor stages (III-IV), we propose a novel role of the miR-130b-PPARγ axis in fostering the progression toward more invasive CRCs.
Influence of tumor peroxisome proliferator-activated receptor gamma and delta expression on postoperative mortality of patients undergoing colorectal cancer surgery.
We studied the association of SNPs in the IL-6 (-174G>C), IL-8 (-251T>A), TNFalpha (-308G>A), ICAM-1 (R241G and K469E), and PPARgamma (Pro12Ala) genes and the risk of CRC.
PPARG, the gene encoding the gamma isoform of the peroxisome proliferator-activated receptor (PPARgamma), is highly expressed in normal human pancreatic islet cells, is located at 3p25, and has been reported to sustain loss-of-function mutations in human colorectal carcinomas.
<b>Purpose:</b> Functional variants in the <i>peroxisome proliferator-activated receptor gamma</i> (<i>PPARG</i>) and <i>PPARG co-activator 1</i> (<i>PPARGC1</i>) family (e.g., <i>PPARGC1A</i> and <i>PPARGC1B</i>) genes were predicted to confer susceptibility to colorectal cancer (CRC).
Together, these results suggest that miR-145 is a novel target of PPARγ, acts as a tumor suppressor in CRC cell lines and is a key regulator of intestinal cell differentiation by directly targeting SOX9, a marker of undifferentiated progenitors in the colonic crypts.
We report a novel PPARG germline mutation in a patient affected by colorectal cancer that replaces serine 289 with cysteine in the mature protein (S289C).
No evidence that polymorphisms in CYP2C8, CYP2C9, UGT1A6, PPARdelta and PPARgamma act as modifiers of the protective effect of regular NSAID use on the risk of colorectal carcinoma.
Although PPARgamma agonists may not by themselves be capable to induce clinical tumor regression, their combination with chemotherapy drugs or other targeted therapies is worth pursuing in the treatment of colorectal carcinoma.