Abstract
In this study, laryngeal tumor cells were killed through the production of excessive reactive oxygen species (ROS) and Ca2+ influx by cisplatin (CISP). Nevertheless, a resistance was determined against CISP treatment in the tumor cells. We have investigated the stimulating role of curcumin (CURC) on CISP-induced human laryngeal squamous cancer (Hep2) cell death through TRPM2 channel activation, and its protective role against the adverse effects of CISP in normal kidney (MPK) cells. Hep2 and MPK cells were divided into four groups as control group, CURC group (10μM for 24 hrs), CISP group (25 μM for 24 hrs), and CURC + CISP combination group. CISP-induced decrease of cell viability, cell count, glutathione peroxidase and glutathione level in Hep2 cells were further increased by CURC treatment, but the CISP-induced normal MPK cell death was reduced by the treatment. CISP-induced increase of apoptosis, Ca2+ fluorescence intensity, TRPM2 expression and current densities through the increase of lipid peroxidation, intracellular and mitochondrial oxidative stress were stimulated by CURC treatment. In conclusion, CISP-induced increases in mitochondrial ROS and cell death levels in Hep2 cells were further enhanced through the increase of TRPM2 activation with the effect of CURC treatment. CISP-induced drug resistance in Hep2 cells might be reduced by CURC treatment.
Highlights
In this study, laryngeal tumor cells were killed through the production of excessive reactive oxygen species (ROS) and Ca2+ influx by cisplatin (CISP)
TRPM2 activation, and intracellular and mitochondrial ROS production were further enhanced by CURC treatment, while cell viability and GSPx were further decreased by the combination (CISP + CURC) treatment
The current results are the first to compare the effect of CURC on CISP-induced TRPM2 channel activation and cell death through excessive ROS production in Hep[2] tumor cells (Fig. 8)
Summary
Laryngeal tumor cells were killed through the production of excessive reactive oxygen species (ROS) and Ca2+ influx by cisplatin (CISP). We have investigated the stimulating role of curcumin (CURC) on CISP-induced human laryngeal squamous cancer (Hep2) cell death through TRPM2 channel activation, and its protective role against the adverse effects of CISP in normal kidney (MPK) cells. CISP-induced increases in mitochondrial ROS and cell death levels in Hep[2] cells were further enhanced through the increase of TRPM2 activation with the effect of CURC treatment. Thereby, about 30% of the patients do not respond to initial CISP treatment due to this imbalance[5,7,8] CISP-induced drug resistance was resolved through the increase of ROS production and Ca2+ influx in several tumor cells except laryngeal squamous cell carcinoma by the use of some antioxidant supplements such as selenium and alpha lipoic acid[9,10,11]. We have evaluated the possible molecular signaling pathway underlying this effectiveness
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