AI Article Synopsis
- Akt-dependent FOXO3a translocation to the cytoplasm helps cancer cells avoid apoptosis, promoting tumor growth.
- The study explored the effects of a non-phosphorylatable FOXO3a mutant on follicular thyroid carcinoma (FTC) cell lines.
- Results showed that introducing this FOXO3a mutant led to cell cycle arrest and apoptosis in FTC cells, and reduced tumor growth in mice, suggesting potential as a gene therapy for FTC.
Article Abstract
Akt-dependent FOXO3a cytoplasmic translocation is an important tumorigenic mechanism for escaping from apoptosis in cancer cells. In the present study, we examined whether non-phosphorylatable FOXO3a can inhibit cell growth of various follicular thyroid carcinoma (FTC) cell lines. Adenovirus carrying the FOXO3a-triple mutant (TM) sequence including point mutations at three Akt phosphorylation sites (Ad-FOXO3a-TM) was generated and transduced to the cells to mimic inhibition of Akt/FOXO3a signal. Transduction of Ad-FOXO3a-TM to FTC133 cells induced cell cycle arrest and apoptosis. Injection of Ad-FOXO3a-TM suppressed the growth of xenograft tumors in athymic mice. Consequently, our results indicate that gene therapy based on Ad-FOXO3a-TM has therapeutic potential for FTC.
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| http://dx.doi.org/10.1016/j.canlet.2011.09.010 | DOI Listing |
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