HIV protease inhibitors block Akt signaling and radiosensitize tumor cells both in vitro and in vivo.

Journal article

In tumor cells with mutations in epidermal growth factor receptor (SQ20B), H-Ras (T24), or K-Ras (MIAPACA2 and A549), the inhibition of Akt phosphorylation increases radiation sensitivity in clonogenic assays, suggesting that Akt is a potential molecular target when combined with therapeutic radiation. Insulin resistance and diabetes are recognized side effects of HIV protease inhibitors (HPIs), suggesting that these agents may inhibit Akt signaling. Because activation of the phosphatidylinos...

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Authors: Gupta, A; Cerniglia, G; Mick, R; Mckenna, W; Muschel, R

• Publication status: Published
• Journal: Cancer research
• Volume: 65
• Issue: 18
• Pages: 8256-8265
• Publication date: 2005-09-01
• DOI: 10.1158/0008-5472.can-05-1220
• EISSN: 1538-7445
• ISSN: 0008-5472
• Language: English
• Keywords: Cell Growth Processes; Phosphorylation; Down-Regulation; Xenograft Model Antitumor Assays; Fibroblasts; Dose-Response Relationship, Drug; Random Allocation; Rats; Signal Transduction; Proto-Oncogene Proteins c-akt; HIV Protease Inhibitors; Mice; Animals; Mice, Nude; Neoplasms; Cell Line, Tumor; Radiation Tolerance; Humans; Radiation-Sensitizing Agents