Rapid CommunicationActivation of PPARγ leads to inhibition of anchorage-independent growth of human colorectal cancer cells☆,☆☆,★
Section snippets
Cell culture
Caco-2, HCT-15, and HCT-116 cells were purchased from American Type Culture Collection (Rockville, MD). HCA-7 cells were a kind gift of Susan Kirkland (University of London).16 Cell lines were grown in Dulbecco's modified Eagle medium (DMEM; GIBCO-BRL, Gaithersburg, MD) supplemented with 10% fetal bovine serum (FBS; Hyclone, Logan, UT), L-glutamine (2 mmol/L), penicillin (100 U/mL), and streptomycin (100 μg/mL) in a 5% CO2 atmosphere with constant humidity.
Stable cell lines
Murine PPARγ 1 complementary DNA
Results and discussion
We selected 4 colon cancer cell lines (HCA-7, HCT-15, HCT-116, and Caco-2) to assess PPARγ expression and endogenous activity. PPARγ mRNA (Figure 1A) and protein (Figure 1B) are present in all 4 cell lines.
Acknowledgements
The authors thank Ron Evans for providing the PPARγ expression vector and the PPRE3-tk-luciferase vector; J. K. Reddy for providing the PPARα expression vector; G. A. Rodan for providing the PPARβ expression vector; and Glaxo Welcome for providing BRL 49653.
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Address requests for reprints to: Raymond DuBois, M.D., Ph.D., Department of Medicine/GI, MCN C-2104, Vanderbilt University Medical Center, Nashville, Tennessee 37232-2279. Fax: (615) 343-6229.
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Supported by U.S. Public Health Services grants DK-47297 to (R.N.D.), NIEHS-00267, and a Veterans Administration Merit Grant to (R.N.D.).
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Dr. DuBois is the Mina Cobb Wallace Professor of Gastroenterology and Cancer Prevention at Vanderbilt University Medical Center.