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Copyright by Eunyoung Park 2007 - The University of Texas at Austin

Copyright by Eunyoung Park 2007 - The University of Texas at Austin

FIGURE 1.2. A. RETINOID

FIGURE 1.2. A. RETINOID METABOLISM (34) AND B. SIGNALING VIA RAR, RXR AND RARE 11

Chapter 2: Retinol Inhibits the Growth of All-Trans-Retinoic Acid- Sensitive and -Resistant Colon Cancer Cells through a Retinoic Acid Receptor-Independent Mechanism ABSTRACT Retinol (vitamin A) is thought to exert its effects through the actions of its metabolite, all-trans-retinoic acid (ATRA), on gene transcription mediated by retinoic acid receptors (RAR) and retinoic acid response elements (RARE). However, RA- resistance limits the chemotherapeutic potential of ATRA. We examined the ability of retinol to inhibit the growth of ATRA-sensitive (HCT-15) and ATRA-resistant (HCT- 116, SW620, and WiDr) human colon cancer cell lines. Retinol inhibited cell growth in a dose-responsive manner. Retinol was not metabolized to ATRA or any bioactive retinoid in two of the cell lines examined. HCT-116 and WiDr cells did convert a small amount of retinol to ATRA, however this amount of ATRA was unable to inhibit cell growth. To show that retinol was not inducing RARE-mediated transcription, each cell line was transfected with pRARE-CAT (chloramphenicol acetyltransferase) and treated with ATRA and retinol. Although treatment with ATRA did increase CAT activity five-fold in ATRA-sensitive cells, retinol treatment did not increase CAT activity in any cell line examined. To demonstrate that growth inhibition due to retinol treatment was independent of ATRA, RAR, and RARE, a pan RAR-antagonist was used to block RAR- signaling. Retinol-induced growth inhibition was not alleviated by the RAR-antagonist 12

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