Curcumin enhances cisplatin-induced human laryngeal squamous cancer cell death through activation of TRPM2 channel and mitochondrial oxidative stress

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作者
Sinem Gökçe Kütük
Gökçen Gökçe
Mustafa Kütük
Hacer Esra Gürses Cila
Mustafa Nazıroğlu
机构
[1] Aydın State Hospital,Department of Otorhinolaryngology
[2] Ankara University,Department of Histology and Embryology, Faculty of Medicine
[3] Aydın State Hospital,Department of Anesthesiology and Reanimation
[4] Hacettepe University,Department of Molecular Metabolism, Faculty of Medicine
[5] Suleyman Demirel University,Department of Biophysics, Faculty of Medicine
[6] Drug Discovery Unit,undefined
[7] BSN Health,undefined
[8] Analysis and Innovation Ltd. Inc. Teknokent,undefined
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Scientific Reports | / 9卷
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摘要
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.
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