SIGNIFICANCE: These findings show that PPARδ contributes to colorectal cancer metastasis by expanding the CSC population, indicating that antagonists that target PPARδ may be beneficial in treating colorectal cancer.
Identification of 15-LOX-1 suppression of PPAR-δ to inhibit IL-6/STAT3 signaling-driven CAC tumorigenesis provides mechanistic insights that can be used to molecularly target CAC.
Peroxisome proliferator-activated receptor δ gene (PPARδ) is correlated with carcinogenesis of colorectal cancer, but the regulation of its gene transcription remains unclear.
Together, these findings consistently indicate that PPAR-beta may facilitate differentiation and inhibit the cell-fibronectin adhesion of colon cancer, having a role as an inhibitor in the carcinogenesis and progression of colorectal cancer.
We conducted this study to evaluate the impact of the expression of peroxisome proliferator-activated receptor delta on angiogenesis in tissue samples of colorectal cancer.
Emerging evidence demonstrates that the peroxisome proliferator-activated receptor delta (PPARdelta) is a focal point of crosstalk between the signaling cascades involved in the progression of colorectal cancer.