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Chronic Inflammation Promotes Retinoblastoma Protein Hyperphosphorylation and E2F1 Activation

¹ Laboratory of Inflammatory-Driven Carcinogenesis, Department of Basic Pharmaceutical Sciences, South Carolina College of Pharmacy; ² Department of Biological Sciences; ³ WJB Dorn Veterans Affairs Medical Center and the School of Medicine, University of South Carolina, Columbia, South Carolina; and ⁴ Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland

Requests for reprints: Lorne J. Hofseth, Department of Basic Pharmaceutical Sciences, College of Pharmacy, University of South Carolina Columbia, Coker Life Sciences, Room 513C, 770 Sumter Street, Columbia, SC 29208. Phone: 803-777-6627; Fax: 803-777-8356; E-mail: hofseth{at}cop.sc.edu.

Chronic inflammation contributes to tumorigenesis. The retinoblastoma protein (pRb), in its hyperphosphorylated form, releases E2 promoter binding factor-1 (E2F1), which drives cell proliferation. Here, we show that pRb is hyperphosphorylated in both mouse and human colitis. In turn, pRb hyperphosphorylation is associated with release of E2F1 from pRb, resulting in the activation of E2F1 target molecules involved in proliferation and apoptosis. These observations provide insight into the in vivo mechanisms associated with chronic colon inflammation and increased colon cancer risk.

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