Abstract
Alcohol increases the risk of carcinoma originated from oral epithelium, but the biological effects of ultra-low doses of ethanol on existing carcinoma cells in combination with natural substances are still unclear. A role for ethanol (EtOH), taken in small amounts as an ingredient of some beverages or mouthwashes to change the growth behavior of established squamous cell carcinoma, has still not been examined sufficiently. We designed an in vitro study to determine the effect of caffeic acid (CFA) on viability and migration ability of malignant oral epithelial keratinocytes, exposed to ultra-low concentrations (maximum 100 mmol/L) EtOH. MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-dimethyltetrazolium bromide) and LDH (lactate dehydrogenase) assays were used to assess the cytotoxic effect of EtOH/CFA and the viability of squamous carcinoma SCC-25 cells (ATCC CRL-1628, mobile part of the tongue). Tested EtOH concentrations were: 2.5, 5, 10, 25, 50, and 100 mmol/L, along with an equal CFA concentration of 50 μmol/L. Carcinoma cells’ migration was investigated by monolayer “wound” healing assay. We demonstrated that very low concentrations of EtOH ranging between 2.5 and 10 mmol/L may induce the viability of oral squamous cell carcinoma cells, while the results following addition of CFA reveal an antagonistic effect, attenuating pro-proliferative EtOH activity. The migration rate of oral squamous carcinoma cells can be significantly inhibited by the biological activity of caffeic acid.
Highlights
Diet of individuals, habits, exposure to environmental chemicals and genetic susceptibility based upon polymorphic variations among genes affect allelic mutations, type and quantity of DNA damage in oral keratinocytes [1]
Epidemiological data have established an etiologic association between exposure to ethyl alcohol (EtOH) and oral mucosa incidence of malignant transformation and oral squamous cell carcinoma (OSCC), but there is still a need to further evaluate this relationship with a focus upon established malignant cell types, within the oral environment enriched with extrinsic substances exhibiting biological activity
Our study was designed to research the pro-proliferative effect of EtOH alone and to determine for the first time, whether the addition of active phenolic substance Caffeic acid (CFA) may attenuate the cancer-promoting effect of ethanol
Summary
Habits, exposure to environmental chemicals and genetic susceptibility based upon polymorphic variations among genes affect allelic mutations, type and quantity of DNA damage in oral keratinocytes [1]. It is well proven that excessive ethanol consumption increases the risk and growth of neoplastic lesions of the oral soft tissues, but the biological effects of short exposure of epithelial cells to ultra-low concentrations of ethanol (EtOH) in combination with some natural substances, are still unclear and undiscovered. Has not been fully established, several potentially important drug-related activities have been reported [8,9,10] Another form of CFA—caffeic acid phenethyl ester (CAPE)—an active component of propolis, has been implicated in the regulation of cell growth and apoptosis [11,12]. Epidemiological data have established an etiologic association between exposure to ethyl alcohol (EtOH) and oral mucosa incidence of malignant transformation and OSCC, but there is still a need to further evaluate this relationship with a focus upon established malignant cell types, within the oral environment enriched with extrinsic substances exhibiting biological activity. The effect of selected concentrations of EtOH and CFA on oral cancer cell motility and migration was evaluated simultaneously
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