Abstract
We studied the effect of lignocaine (LIG) on lung cancer cells. LIG dose- and concentration-dependently reduced the viability of the lung cancer cell line 95D. Fluorescence microscopy revealed that LIG-induced apoptosis, and this was confirmed via flow cytometric analysis of cells treated with various concentrations of LIG; the drug increased the proportions of cells in S-phase. Bad and Bax levels rose, and that of Bcl2 fell significantly, after addition of LIG; Western blotting showed that the drug also reduced the levels of phosphorylated proteins involved in downstream phosphoinositide 3-kinases/mammalian target of rapamycin/mammalian target of rapamycin signaling. In conclusion, our results suggest that LIG may be a useful therapy for human lung carcinoma.
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