Peroxisome Proliferator-activated Receptor ¦Ä (ppar¦Ä Is) The Role Of Research In Colorectal Carcinogenesis

PURPOSE: To clarify the expression change of Peroxisome proliferator-activated receptorδ(PPARδ) gene in human colorectal cancer tissues, and determine the correlation of PPARδexpression with clinical and pathological parameters of colorectal cancer. METHODS: Applying Real-time RT-PCR, we quantified PPARδmRNA in 86 tissues from excised primary rectal cancers. In each case, accompanying normal mucosa was collected for comparison.RESULTS: Among the 86 rectal cancer tissues, 55.8% (48/86) cases showed PPARδoverexpression: 45.3% (39/86) tumors gave an expression level 1.5 to 5.0 times, 5.8% (5/86) tumors 10 to 20 times, and 4.7% (4/86) tumors more than 20 times relative to normal mucosa. However, the general level of PPARδmRNA in rectal cancer tissues is not statistically different from normal mucosa. No significant links were found between PPARδexpression and cell differentiations, pathological categories and Dukes stages.CONCLUSIONS: The expression of PPARδgene in rectal cancers is not statistically different from normal mucosa, and it doesn't correlate with cell differentiation, pathological categories and Dukes stages. PURPOSE: To investigate the effects of peroxisome proliferator-activated receptorδ(PPARδ) on the proliferation and apoptosis of human colorectal cancer (CRC) cells.METHODS: For RNA interfering (RNAi), HCT-116 cells were transfected with short hairpin RNA (shRNA)-expressing plasmids against PPARδor negative control vectors. The efficacy of RNAi was assessed by real-time reverse transcription polymerase chain reaction (RT-PCR). The proliferation, cell cycle and apoptosis of HCT-116 cells treated by RNAi, compared with those containing control vectors or untreated, were analyzed respectively using MTT (methyl thiazolyl tetrazolium), flow cytometry (FCM) and TdT (terminal deoxynucleotidyl transferase)-mediated dUTP nick end-labeling (TUNEL) assay.RESULTS: RNAi targeting PPARδresulted in substantial suppression of PPARδexpression and significantly promoted the proliferation of HCT-116 cells relative to those with control vectors or untreated, obviously decreasing the frequency of G₁-phase cells, but had no effect on cell apoptosis.CONCLUSIONS: PPARδmay inhibit the proliferation of CRC cells and increase the number of G₁-phase cells, without any function in cellapoptosis, which suggests an inhibitive role of PPARδgene in colorectalcarcinogenesis.