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Regulation of CD36 expression in human melanoma cells
Min Chen1, Erica Pych, Cyndy Corpron
1Department of Surgery, University of Michigan, F3970 Mott Hospital, Ann Arbor, MI 48109-0245, USA.
Background:
CD36 is a suspected facilitator of long chain fatty acid transport and as a thrombospondin (TSP) receptor, thereby being implicated in cell proliferation, angiogenesis and tumor metastasis. The human amelanotic melanoma cell line, C32, is known to express CD36 and has been as a model for studying TSP binding.
Purpose:
The purpose of this study was to investigate the regulation of CD36 expression in the C32 cell line.
Method:
C32 cells were treated with 12-O-tetradecanoylphorobol-13-acetate (TPA)(10 microM), insulin (174 nM), ibuprofen (0.3 mM) and oleic acid. CD36 mRNA levels were determined by Northern Blot analysis using human CD36 cDNA probe. Western blot analysis utilized the human anti-CD36 antibody. Protein and mRNA concentration was determined by autoradiography, densitometry and NIH image software. Statistical analysis was by Student's t-test with P < 0.05 considered significant.
Results:
CD36 mRNA levels were decreased 2.2 fold in C32 cells treated with TPA (p < 0.05) compared to control cells. Insulin treated cells showed a 30% increase (p < 0.05) in CD36 mRNA levels. Ibuprofen, a regulator of peroxisomal proliferation activated receptor (PPAR) alpha, was found to increase CD36 protein levels by 50% (p < 0.05). Oleic acid had no effect on CD36 mRNA or protein levels.
Conclusion:
The finding that the tumor promoter TPA significantly decreases CD36 mRNA levels, while insulin and ibuprofen increase CD36 expression, may have important implications in tumor biology. The regulation of CD36 expression in tumor cells may play an important role in tumor growth, metastasis and angiogenesis.