Abstract |
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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Authors | Chung-Yi Chen, Yi-Wen Li, Soong-Yu Kuo |
Journal | Molecules (Basel, Switzerland)
(Molecules)
Vol. 14
Issue 3
Pg. 959-69
(Mar 02 2009)
ISSN: 1420-3049 [Electronic] Switzerland |
PMID | 19255554
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antineoplastic Agents
- Calcium Channels, L-Type
- Catechols
- Fatty Alcohols
- gingerol
- Protein Kinase C
- Calcium
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Topics |
- Antineoplastic Agents
- Calcium
(metabolism)
- Calcium Channels, L-Type
- Catechols
(pharmacology, therapeutic use)
- Cell Survival
(drug effects)
- Colorectal Neoplasms
(drug therapy, pathology)
- Endoplasmic Reticulum
(metabolism)
- Fatty Alcohols
(pharmacology, therapeutic use)
- Humans
- Protein Kinase C
(metabolism)
- Tumor Cells, Cultured
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