| Project/Area Number |
15590061
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
TAHARA Hidetoshi Hiroshima University, Graduated School of Biomedical Sciences, Associate Professor, 大学院・医歯薬学総合研究科, 助教授 (00271065)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2004: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2003: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | telomerase / telomere / anti-cancer drug / anti-aging drug / hTERT / regenerative tissues / MEN1 / ルシフェラーゼ / 不死化 / 制ガン剤 / がん細胞 / セルソーター / GFP / cDNA |
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| Research Abstract |
Telomerase activity was regulated by hTERT gene regulation. hTERT promoter (1.8kbp) was cloned into reporter vector which can monitoring hTERT transcription by green fluorescence or luciferase activity. Since normal fibroblasts have limited life span, normal fibroblasts need to be immortalized to using monitoring cells. hTERT gene was infected with retroviruses to immortalized cells. hTERT immortalized normal fibroblasts, NHF-hTERT and MRC-hTERT were used to generate hTERT transcription monitoring cells. We finally generated NHFT-TRP-Luc and MRCT-TRPLuc. We also constructed monitoring cell, RKO-TRPLuc, derived from telomerase positive cancer cells to screening anti-cancer drug targeted hTERT transcription. Using RKO-TRPluc cells, we screened natural compounds which suppress hTERT transcription in cancer cells, and 12 natural products were identified. Among them, two samples showed strong inhibition of hTERT transcription. These two compounds should be powerful anti-cancer activity. Further examination should be necessary to clarify the mechanism of these compounds.
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