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- W2968600130 abstract "3406 In RCC cell lines, we found by real-time RT-PCR that EGFR mRNA was highly expressed in the near-absence of other ErbB family members. Based on these findings, we used a selective EGFR inhibitor. Iressa, alone and in combination with rapamycin to inhibit growth. Synergy was observed with the combination but only in wt-VHL cells. Short-term (2h) treatment with Iressa blocked ERK1, 2 phosphorylation specifically in wt-VHL cells while rapamycin inhibited phospho-RPS6 irrespective of VHL. Neither agent, nor the combination, affected phospho-AKT levels. Although the ability to block EGFR phosphorylation was VHL independent, in matched cell lines EGFR protein was overexpressed and EGF-induced phosphorylation was prolonged in VHL mutant cells. The elevated EGFR protein levels were not due to differences in total or ribosome-associated mRNA indicating a post-translational effect. We also determined whether Iressa and rapamycin had effects on protein translation initiation for other mRNAs. While 5’-TOP containing mRNAs were inhibited (e.g., RPS19), as well as eIF4E, no changes were observed for MYC, Cyclin D1 and VEGF. In contrast, following short-term inhibition of AKT phophorylation with LY-294002, polysome-associated MYC mRNAs was substantially downregulated and mRNAs for Cyclin D1 and VEGF were downregulated in total RNA with effects being greater in cells with wt-VHL. We conclude that combined EGFR and mTOR inhibitors may be effective in RCCs with wt-VHL and that non-ErbB kinases are likely responsible for maintaining AKT phosphorylation. The inability to alter AKT phosphorylation may limit the anti-tumor effects of Iressa plus rapamycin." @default.
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- W2968600130 date "2005-05-01" @default.
- W2968600130 modified "2023-09-23" @default.
- W2968600130 title "Synergistic growth inhibition by Iressa and Rapamycin in Renal Cell Carcinoma (RCC) with wild-type VHL" @default.
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