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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Amidines, Animals, Arachidonic Acid, Carcinoma, Renal Cell, Cell Growth Processes, Cytochrome P-450 Enzyme System, Cytochrome P450 Family 4, Down-Regulation, Humans, Hydroxyeicosatetraenoic Acids, Kidney Neoplasms, Mice, Mice, Nude, RNA, Messenger, TNF-Related Apoptosis-Inducing Ligand, Xenograft Model Antitumor Assays.
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Does down-regulation of 20-HETE synthesis and signaling inhibit renal adenocarcinoma cell proliferation and tumor growth? Context: We examined the ability of inhibitors of the synthesis or actions of 20-HETE, metabolite of arachidonic acid, to inhibit proliferation of human renal carcinoma cell lines. 786-O and 769-P cells were exposed to either 10 microM HET0016 (selective inhibitor of 20-HETE synthesis), 10 microM WIT002 (20-HETE antagonist), or vehicle. Subsequently, we assessed the effect of WIT002 on tumor growth in vivo using an ectopic mouse model of clear-cell renal carcinoma. Addition of HET0016 and WIT002 inhibited the proliferation of 786-O and 769-P human renal cell carcinoma lines. HET0016 and WIT002 had little effect on the proliferation of primary cultures of normal human proximal tubule epithelial cells. WIT002 (10 mg/kg, s.c.) administered daily to athymic nude mice implanted subcutaneously with 786-O cells reduced the growth of the tumors by 84 % compared to vehicle (p<0.001).
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20-HETE is required for proliferation of human renal epithelial cancer. Final Decision: yes