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https://doi.org/10.6342/ntu.2008.01072
Copy DOIPublication Date: Sep 11, 2008 |
Lung cancer is very difficult to be cured even using target gene therapy. In East Asia’s non-smoking women Iressa and Tarceva, two newly developed EGRF tyrosine kinase inhibitor (EGFR TKIs), largely reduce the tumor size in 77% patients in a few weeks time. In most of the lung patients who treated with EGFR TKIs, however, it is very disappointing that the cancer is recurrent within 6-12 months with drug resistance (Sharma et al., 2007). Iodoacetic acid (IAA) is not only an inhibitor of GAPDH but also plays a crucial role in variety novel cellular functions. Using human lung cancer cell lines, I investigated possible mechanism(s) of IAA-induced cell death. My results showed that IAA induced dose-dependent cell death, including A549, NCI HOP62, NCI H23 NCI EKVX, H522 and H1299. I also found that IAA induced cytochrome c release, caspase-3 activation, and chromatin condensation in A549. Furthermore, IAA induced intracellular ATP and GSH depletion, and pretreatment with either NAC or DTT prevented IAA-induced cell death. In conclusion, my data demonstrated that IAA effectively induced cell death in at least six lung cancer cell lines. It might provide possible target therapy for future clinical use.
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