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• W2152334650 endingPage "2840" @default.
• W2152334650 startingPage "2831" @default.
• W2152334650 abstract "Abstract Intracellular supply of dTTP is a highly regulated process and has been a key target for chemotherapeutic drug development. Thymidylate kinase (TMPK) is the key enzyme for dTTP formation in both de novo and salvage pathways. In this study, we used lentiviral-based small hairpin RNA to silence TMPK expression in p53(+/+) and p53(−/−) HCT-116 colon cancer cells. This approach was sufficient to decrease the dTTP pool gradually without affecting p53 expression and generating cytotoxicity. TMPK knockdown significantly increased doxorubicin sensitivity dramatically in p53-proficient, p53-null HCT-116, and LoVo colon cancer cells. The decrease in the dTTP pool using this approach augmented the DNA damage response and enhanced apoptotic induction after exposure to low-dose doxorubicin, leading to cell death. In contrast, silencing of thymidylate synthase which blocks the de novo pathway was incapable of sensitizing p53-null HCT-116 cells to doxorubicin-induced apoptosis because of the compensation by the salvage pathway. Our results suggest the lentiviral delivery of small hairpin RNA targeting TMPK in combination with a low dose of doxorubicin as a new approach to kill colon cancer cells regardless of p53 status. [Cancer Res 2008;68(8):2831–40]" @default.
• W2152334650 created "2016-06-24" @default.
• W2152334650 creator A5039591687 @default.
• W2152334650 creator A5049073157 @default.
• W2152334650 date "2008-04-15" @default.
• W2152334650 modified "2023-10-09" @default.
• W2152334650 title "Synthetic Lethality by Lentiviral Short Hairpin RNA Silencing of Thymidylate Kinase and Doxorubicin in Colon Cancer Cells Regardless of the <i>p53</i> Status" @default.
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• W2152334650 doi "https://doi.org/10.1158/0008-5472.can-07-3069" @default.
• W2152334650 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18413751" @default.
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