THE CYTOTOXIC EFFECT OF BENZOIC ACID ON TEN DIFFERENT CANCER CELL LINES
Abstract
Cancer, having numerous types, is among the most dangerous and complex chronic diseases in the world affecting the wellbeing of humans, society and economy. The exploration and reassessment of effective chemicals, compounds, and natural products as potential agents for alleviating the adverse effects of cancer and its related symptoms continue on a global scale. This process involves an initial evaluation of the cytotoxic activities of potential drug candidates or treatment regimens on diverse cancer cell types in an ex vivo context. Benzoic acid (BA), an aromatic carboxylic acid that is widely available and used in the food industry, is one of the phenolic acids that may bear considerable anti-cancer potential. It is useful to find out the comparable effect of BA on various cancer types. Therefore, in this study, we tested the cytotoxicity of BA using MTT assay, on a number of ten different cancer cell lines and one normal cell type, namely prostate cancer (PC3), cervical cancer (HeLA), liver cancer (HUH7), colon cancer (CaCO2, HT29, SW48), bone cancer (MG63 and A673), pharyngeal cancer (2A3), lung cancer (CRM612) and kidney epithelial control cell line (Phoenix), respectively. IC50 (µg/ml) values after 48 and 72-hour exposure to BA were found to differ between 85.54±3.17 to 670.6±43.26, while the IC values for the control cell line Phoenix were 410.54±32.29 and 231.16±25.25, respectively. Taking into account of statistical evaluation of the IC50 values for BA on 11 cell types, we suggest that the molecular and omics approaches can be implemented in more details in order to find cellular and biochemical targets of BA as well as elucidating molecular mode of action, especially starting with the cancer cell lines of MG63, CRM612 and A673, in which the IC50 levels are relatively the lowest compared to those of the control cell line.
Keywords
Benzoic acid, Cytotoxic effect, Anticancer, MTT
Thanks
This study, Biotechnology Research Center and Proteogenome Technologies research laboratory at Mugla Sitki Kocman University Research Laboratories Center provided support in Turkey. Their support was gratefully acknowledged.
References
- [1] Hanahan D, Weinberg RA. The hallmarks of cancer. Cell 2000; 100(1), 57-70. https://doi.org/10.1016/S0092-8674(00)81683-9
- [2] Lund AH, van Lohuizen M. Epigenetics and cancer. Genes Dev 2004; 18(19), 2315-2335
- [3] Sung H, Ferlay J, Siege RL, Laversanne M, et al. Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA-Cancer J Clin 2021; 71(3), 209-249.
- [4] Oto Murat. Osteosarkom ve varyantlarına tanısal yaklaşım modaliteleri. Pamukkale Tıp Dergisi 2008; (1), 59-64.
- [5] Cho WH, Lee HJ, Choi YJ, Oh JH, Kim HS, Cho HS. Capsaicin induces apoptosis in MG63 human osteosarcoma cells via the caspase cascade and the antioxidant enzyme system. Mol Med Rep 2013; 8(6), 1655-1662.
- [6] Wang M, Yin B, Wang HY, Wang RF. Current advances in T-cell-based cancer immunotherapy. Immunotherapy 2014; 6(12), 1265-1278.
- [7] Anantharaju PG, Gowda PC, Vimalambike MG, Madhunapantula SV. An overview on the role of dietary phenolics for the treatment of cancers. Nutr J 2016; 15(1), 1-16.
- [8] Devi KP, Rajavel T, Habtemariam S, Nabavi SF, Nabavi SM. Molecular mechanisms underlying anticancer effects of myricetin. Life Sci 2015; 142, 19-25.
- [9] Kennedy DO, Wightman EL. Herbal extracts and phytochemicals: plant secondary metabolites and the enhancement of human brain function. Adv Nutr 2011; 2(1), 32-50.
- [10] Soto-Vaca A, Gutierrez A, Losso JN, Xu Z, Finley JW. Evolution of phenolic compounds from color and flavor problems to health benefits. J Agr Food Chem 2012; 60(27), 6658-6677.