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- W2117755372 abstract "Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FLSecondary bile acids have long been thought to influence the etiology of colon tumorigenesis however, the mechanism of their action remains unclear. Our previous studies focused on deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA) because they appear to have the opposite effect at the molecular and the biological level. DCA stimulates mitogenic signaling by activating the EGF receptor and can promote tumorigenesis in mouse models, whereas UDCA suppresses EGFR-related mitogenic signaling and has been shown to inhibit colon tumorigenesis in clinical trials. In previous studies we showed that both bile acids act on the cell membrane and this resulted in stimulation of EGFR activity by DCA, but resulted in suppression of receptor signaling by UDCA. In this work, the effect of DCA and UDCA on EGFR internalization in Hct116 cells was investigated using reverse biotinylation. Both DCA and UDCA were found to induce ligand independent internalization of EGFR. However, UDCA treatment resulted in rapid degradation of EGFR whereas DCA caused internalization and stabilization of the receptor in an apparently activated state. To examine this further we pretreated the cells with Methyl-β-cyclodextrin to deplete cholesterol from the plasma membrane, or with chlorpromazine to inhibit endocytosis through clatherin coated pits (CCP). We also suppressed functioning of caveolae or CCPs using caveolin-1 shRNA, or clathrin heavy chain shRNA. We found that EGFR internalization induced by UDCA is cholesterol and caveolin dependent. However, none of these treatments affected the rate of EGFR internalization induced by DCA, suggesting that DCA induced EGFR internalization by a mechanism which is different from that of either EGF or UDCA. This may explain the distinct biological activities exhibited by these two bile acids.Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1202. doi:10.1158/1538-7445.AM2011-1202" @default.
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- W2117755372 date "2011-04-15" @default.
- W2117755372 modified "2023-09-27" @default.
- W2117755372 title "Abstract 1202: DCA induces EGFR internalization by a mechanism that is distinct from EGF or UDCA" @default.
- W2117755372 doi "https://doi.org/10.1158/1538-7445.am2011-1202" @default.
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