Abstract
The candidate tumor suppressor fragile histidine traid (FHIT) is frequently inactivated in small cell lung cancer (SCLC). Mutations in the p53 gene also occur in the majority of SCLC leading to the accumulation of the mutant protein. Here we evaluated the effect of FHIT gene therapy alone or in combination with the mutant p53-reactivating molecule, PRIMA-1(Met)/APR-246, in SCLC. Overexpression of FHIT by recombinant adenoviral vector (Ad-FHIT)-mediated gene transfer in SCLC cells inhibited their growth by inducing apoptosis and when combined with PRIMA-1(Met)/APR-246, a synergistic cell growth inhibition was achieved.
| Original language | English |
|---|---|
| Journal | Cancer Investigation |
| Volume | 29 |
| Issue number | 10 |
| Pages (from-to) | 683-91 |
| Number of pages | 9 |
| ISSN | 0735-7907 |
| DOIs | |
| Publication status | Published - 2011 |
Keywords
- Acid Anhydride Hydrolases
- Adenoviridae
- Apoptosis
- Carcinoma, Small Cell
- Cell Line, Tumor
- Gene Expression
- Gene Therapy
- Humans
- Lung Neoplasms
- Neoplasm Proteins
- RNA, Messenger
- Tumor Suppressor Protein p53
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