The effect of [10]-gingerol on cytosol free Ca
2+ concentration ([Ca
2+]
i) and viability is large unknown. This study examines the early signaling effects of [10]-gingerol on human colorectal cancer cells. It was found that this compound caused a slow
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The effect of [10]-gingerol on cytosol free Ca
2+ concentration ([Ca
2+]
i) and viability is large unknown. This study examines the early signaling effects of [10]-gingerol on human colorectal cancer cells. It was found that this compound caused a slow and sustained rise of [Ca
2+]
i in a concentration-dependent manner. [10]-Gingerol also induced a [Ca
2+]
i rise when extracellular Ca
2+ was removed, but the magnitude was reduced by 38%. In a Ca
2+-free medium, the [10]-gingerol-induced [Ca
2+]
i rise was partially abolished by depleting stored Ca
2+ with thapsigargin (an endoplasmic reticulum Ca
2+ pump inhibitor). The elevation of [10]-gingerol-caused [Ca
2+]
i in a Ca
2+-containing medium was not affected by modulation of protein kinase C activity. The [10]-gingerol-induced Ca
2+ influx was insensitive to L-type Ca
2+ channel blockers. At concentrations of 10-100 mM, [10]-gingerol killed cells in a concentration-dependent manner. These findings suggest that [10]-gingerol induces [Ca
2+]
i rise by causing Ca
2+ release from the endoplasmic reticulum and Ca
2+ influx from non-L-type Ca
2+ channels in SW480 cancer cells.
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