Cuijuan Wang1, Xingguo Song2, Ming Shang2, Wei Zou1, Mengping Zhang1, Haiyan Wei1, Hua Shao1. 1. Key Laboratory of Public Health, Shandong Academy of Occupational Health & Occupational Medicine, Shandong Academy of Medical Sciences, Jinan, Shandong, PR China. 2. Shandong Provincial Key Laboratory of Radiation Oncology, Shandong Cancer Hospital Affiliated to Shandong University, Shandong Academy of Medical Sciences, Jinan, Shandong, PR China.
Abstract
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.
AIM: Curcumin induces cytotoxic cell death in several humancancer 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.
Entities:
Keywords:
DNA damage; ER stress; curcumin; mitochondrial apoptosis; non-small-cell lung cancer; reactive oxygen species