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Updated: Jun 25, 2026
Quantification of Cytokine-Induced Cell Death in Human Colonic Organoids Using Live Fluorescence Microscopy
Published on: August 2, 2024
Effect of [10]-gingerol on [ca2+]i and cell death in human colorectal cancer cells
Chung-Yi Chen1, Yi-Wen Li, Soong-Yu Kuo
1Department of Medical Technology, School of Medicine and Health Sciences, Fooyin University, Kaohsiung County 83101 Taiwan. xx377@mail.fy.edu.tw
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.
Insights
[10]-gingerol, a compound found in ginger, triggers a rise in intracellular calcium (Ca2+) and cell death in colorectal cancer cells. This occurs through calcium release from the endoplasmic reticulum and influx via non-L-type channels.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- The effects of [10]-gingerol on intracellular calcium ([Ca2+]i) and cancer cell viability are not well understood.
- Colorectal cancer remains a significant global health challenge, necessitating research into novel therapeutic agents.
Purpose of the Study:
- To investigate the early signaling mechanisms of [10]-gingerol in human colorectal cancer cells.
- To determine the impact of [10]-gingerol on intracellular calcium concentration and cell viability.
Main Methods:
- Measurement of intracellular calcium ([Ca2+]i) using fluorescent indicators.
- Experiments conducted in both calcium-containing and calcium-free media.
- Assessment of calcium release from intracellular stores using thapsigargin.
- Evaluation of cell viability following [10]-gingerol treatment at various concentrations.
Main Results:
- [10]-gingerol induced a slow, sustained, and concentration-dependent rise in [Ca2+]i.
- Calcium influx from extracellular sources contributed 38% to the [10]-gingerol-induced [Ca2+]i rise.
- The [10]-gingerol-induced [Ca2+]i rise was partially dependent on endoplasmic reticulum calcium stores and insensitive to protein kinase C modulation.
- [10]-gingerol treatment led to cell death in a concentration-dependent manner (10-100 mM).
Conclusions:
- [10]-gingerol elevates intracellular calcium ([Ca2+]i) in SW480 colorectal cancer cells.
- The mechanism involves calcium release from the endoplasmic reticulum and influx through non-L-type calcium channels.
- [10]-gingerol exhibits cytotoxic effects on colorectal cancer cells, suggesting potential therapeutic applications.