Abstract: Abstract：Objective To study whether carvacrol can cause apoptosis in non-small cell lung cancer (NSCLC) cell line NCI-H1299, and explore its possible molecular mechanism. Methods NCI-H1299 cells were treated with different concentrations of carvacrol (20, 40, 60 and 80 μmol/L) for 24 or 48 h. The viability of cells was evaluated by MTT assay, apoptosis was analyzed by flow cytometry (FCM) and the effect of carvacrol on metastasis of NCI-H1299 was analyzed by Transwell assay. The expression level of caspase-9, MMP-9 and TIMP-1 were detected by quantitative realtime-PCR and Western blot assay. Results After treatment with carvacrol, the viability of NCI-H1299 cells was suppressed dramatically (P<0.05), without dose-dependent manner (P>0.05). After being incubated with carvacrol for 24 h, FCM analysis indicated that carvacrol effectively induced apoptosis in NCI-H1299 cells (P<0.05), without dose-dependent manner (P>0.05). The ability of invasion was decreased (40.67±3.63 vs. 76.00±5.78). Carvacrol inhibited the protein and mRNA expression levels of caspase-9, but increased the expression of MMP-9 and TIMP-1 (P＜0.05). Conclusion Carvacrol can induce apoptosis of NCI-H1299 cells and inhibit their invasion, which may be associated with up-regulation of caspase- 9 expression and down-regulation of MMP-9 expression.

Key words:  carcinoma, non-small-cell lung, apoptosis, neoplasm invasiveness, caspase 9, matrix metalloproteinases 9, tissue inhibitor of metalloproteinases, Carvacrol human non-small cell lung cancer NCI-H1299 cells