Curcumin exerts cytotoxicity dependent on reactive oxygen species accumulation in non-small-cell lung cancer cells

• Published in: Future oncology (London, England) Vol. 15; no. 11; pp. 1243 - 1253
• Main Authors: Wang, Cuijuan, Song, Xingguo, Shang, Ming, Zou, Wei, Zhang, Mengping, Wei, Haiyan, Shao, Hua
• Format: Journal Article
• Language: English
• Published: England Future Medicine Ltd 01.04.2019
• Subjects: Apoptosis; Cancer therapies; Cell cycle; curcumin; DNA damage; Drug delivery systems; Drugs; ER stress; Lung cancer; Metabolism; mitochondrial apoptosis; non-small-cell lung cancer; Oxidative stress; reactive oxygen species; United States > US; China; ER stress; DNA damage; mitochondrial apoptosis; reactive oxygen species; curcumin; non-small-cell lung cancer
• ISSN: 1479-6694; 1744-8301
• DOI: 10.2217/fon-2018-0708

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. 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. 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 -acetyl- -cysteine. Curcumin decreased mitochondrial transmembrane potential and induced ROS production, thereby activating the DNA damage/repair pathway and mitochondrial apoptosis. These results indicate that curcumin could be an effective therapeutic candidate for NSCLC.