S-allylcysteine induces cytotoxic effects in two human lung cancer cell lines via induction of oxidative damage, downregulation of Nrf2 and NF-κB, and apoptosis. Issue 2 (February 2021)

• Record Type: Journal Article
• Authors: Orozco-Morales, Mario; Hernández-Pedro, Norma Yanet; Barrios-Bernal, Pedro; Arrieta, Oscar; Ruiz-Godoy, Luz María; Aschner, Michael; Santamaría, Abel; Colín-González, Ana Laura
• Is Part Of: Anti-cancer drugs. Volume 32:Issue 2(2021)
• Publication Date: 2021-02
• Subjects: apoptotic cell death -- antineoplastic properties -- cytotoxicity -- garlic-derived compound -- lung cancer cell lines; Antineoplastic agents -- Periodicals; Cancer -- Chemotherapy -- Periodicals; Antineoplastic Agents -- therapeutic use -- Periodicals; Drug Therapy -- Periodicals; 616.994061
• DOI: 10.1097/CAD.0000000000001015
• Languages: English
• ISSNs: 0959-4973

Abstract

Abstract : In this study, we investigated the putative cytotoxic effect elicited by the garlic-derived compound S-allylcysteine (SAC) in two human cancer cell lines (HCC827 and NCI-H1975) in order to develop an experimental approach to the therapeutic potential of this molecule for lung cancer. Cells were incubated for 24, 48 and 72 h in the presence of SAC (10 or 20 mM), which resulted in a concentration- and time-dependent decrease in cell viability and culture confluence in both cell lines. These effects were contrasted with – and validated through – those observed in an immortalized but nontumorigenic epithelial cell line from human bronchial epithelium (BEAS-2B, negative control) and an adenocarcinoma human alveolar basal epithelial cell line (A549, positive control). SAC (20 mM at 72 h) also increased the oxidative damage to lipids, augmented apoptosis, and decreased the expression of the nuclear factor erythroid 2-related factor 2 (Nrf2) and the nuclear factor kappa B (NF-κB) proteins in HCC827 and NCI-H1975 cells. Our results establish the efficacy of SAC in reducing malignant growth and proliferation of lung tumor cells. This effect is mediated by the induction of oxidative damage associated with the downregulation of Nrf2 and NF-κB and their corresponding signaling pathways.