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Carcinogenesis, Vol. 22, No. 9, 1379-1383, September 2001
© 2001 Oxford University Press

CANCER BIOLOGY

Activation of the PPAR pathway induces apoptosis and COX-2 inhibition in HT-29 human colon cancer cells

Wan-Lin Yang and Harold Frucht,1

Division of Oncologic Gastroenterology, Fox Chase Cancer Center, Philadelphia, PA 19111, USA

The {gamma} isoform of the peroxisome proliferator-activated receptor (PPAR{gamma}) is a nuclear receptor that regulates adipocyte differentiation. Recently it has been shown to be expressed in human colonic mucosa and cancer, but its role in colon carcinogenesis and progression is still unclear. We demonstrate that activation of PPAR{gamma} by ciglitazone (cig), a selective PPAR{gamma} ligand, induces HT-29 human colon cancer cells to undergo apoptosis. Treatment with cig also down-regulates expression of cyclooxygenase-2 (COX-2) protein. Simultaneous exposure of cells to cig and 9-cis-retinoic acid (9-cis-RA), a ligand for retinoid X receptor, results in an increased apoptotic effect and increased inhibition of COX-2 expression, compared with cells treated with either cig or 9-cis-RA alone. As COX-2 is overexpressed in human colon cancer and has been implicated in augmenting invasiveness and tumorigenecity, the ability of PPAR{gamma} activation to decrease COX-2 expression and induce apoptosis suggests that the PPAR{gamma} pathway may be considered as a therapeutic target for colon cancer.


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