Aim: Curcumin induces cytotoxic cell death in several human cancer cells. Here, we have investigated the effects of curcumin on non-small-cell lung cancer (NSCLC) with an aim to identify underlying mechanisms of its cytotoxic effect.
Materials & methods: The effects of various concentrations of curcumin on the NSCLC cell lines A549 and SPC-A1 were evaluated by MTT assay, colony-forming assay and flow cytometry. Additionally, protein expression associated with different signaling pathways was assessed using western blotting.
Results: Curcumin exhibited cytotoxicity against NSCLC, evident from the inhibition of cell proliferation, G2/M arrest, DNA damage, endoplasmic reticulum stress and mitochondrial apoptosis. The anticancer effect was related to reactive oxygen species (ROS) accumulation and could be reversed by ROS scavengers, catalase and N-acetyl-l-cysteine. Curcumin decreased mitochondrial transmembrane potential and induced ROS production, thereby activating the DNA damage/repair pathway and mitochondrial apoptosis.
Conclusion: These results indicate that curcumin could be an effective therapeutic candidate for NSCLC.
Keywords: DNA damage; ER stress; curcumin; mitochondrial apoptosis; non-small-cell lung cancer; reactive oxygen species.