Gallic acid induces apoptosis in A375.S2 human melanoma cells through caspase-dependent and -independent pathways
- Chyi Lo
- Tung-Yuan Lai
- Jen-Hung Yang
- Jai-Sing Yang
- Yi-Shih Ma
- Shu-Wen Weng
- Ya-Yin Chen
- Jaung-Geng Lin
- Jing-Gung Chung
School of Chinese Medicine, China Medical University, Taichung 404, Taiwan, R.O.C.
- Published online on: August 1, 2010 https://doi.org/10.3892/ijo_00000686
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The natural antioxidant gallic acid (GA) has demonstrated a significant inhibition of cell proliferation and induction of apoptosis in a series of cancer cell lines. However, there is no available information to show whether GA induces apoptosis in human skin cancer cells. In the present study, we report GA-induced apoptosis in A375.S2 human melanoma cells. GA affected morphological changes, decreased the percentage of viable cells and induced apoptosis in A375.S2 cells in a dose- and time-dependent manner. Observation of the molecular mechanism of apoptosis in A375.S2 cells showed that GA up-regulated the proapoptotic proteins such as Bax, and induced caspase cascade activity, but down-regulated antiapoptotic proteins such as Bcl-2. GA induced reactive oxygen species (ROS) and intracellular Ca2+ productions and decreased the level of mitochondrial membrane potential (ΔΨm) in A375.S2 cells in a time-dependent manner. GA triggered cytosolic release of apoptotic molecules, cytochrome c, promoted activation of caspase-9 and caspase-3, and ultimately apoptotic cell death. In addition, GA also promoted cytosolic release of apoptosis-inducing factor (AIF) and endonuclease G (Endo G). Therefore, GA may also induce apoptosis through a caspase-independent pathway. Our results suggest that GA might be a potential anticancer compound; however, in depth in vivo studies are needed to elucidate the exact mechanism.