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Ethyl gallate induces apoptosis of HL-60 cells by promoting the expression of caspases-8, -9, -3, apoptosis-inducing factor and endonuclease G.

Kim WH, Song HO, Choi HJ, Bang HI, Choi DY, Park H - Int J Mol Sci (2012)

Bottom Line: Western blotting analysis indicated that EG-mediated HL-60 apoptosis mainly occurred through the mitochondrial pathway, as shown by the release of cytochrome c, apoptosis-inducing factor (AIF), and endonuclease G (Endo G), as well as the upregulation of Bcl-2-associated X protein (Bax).EG also activated the death receptor-dependent pathway of apoptosis by enhancing the expression of caspases-8, -9, and -3 and the Bcl-2 interacting domain (Bid).Collectively, our results showed that EG induces apoptosis in HL-60 via mitochondrial-mediated pathways.

View Article: PubMed Central - PubMed

Affiliation: Department of Infection Biology, Zoonosis Research Center, Wonkwang University School of Medicine, 344-2, Shinyong-dong, Iksan, Chonbuk 570-749, South Korea; E-Mails: woong621@gmail.com (W.-H.K.); sea5328@daum.net (H.-O.S.); rerived@empal.com (H.-J.C.).

ABSTRACT
Many phytochemicals have been recognized to have potential therapeutic efficacy in cancer treatment. In this study, we investigated ethyl gallate (EG) for possible proapoptotic effects in the human promyelocytic leukemia cell line, HL-60. We examined cell viability, morphological changes, DNA content and fragmentation, and expression of apoptosis-related proteins for up to 48 h after EG treatment. The results showed that EG induced morphological changes and DNA fragmentation and reduced HL-60 cell viability in a dose-dependent and time-dependent manner. Western blotting analysis indicated that EG-mediated HL-60 apoptosis mainly occurred through the mitochondrial pathway, as shown by the release of cytochrome c, apoptosis-inducing factor (AIF), and endonuclease G (Endo G), as well as the upregulation of Bcl-2-associated X protein (Bax). EG also activated the death receptor-dependent pathway of apoptosis by enhancing the expression of caspases-8, -9, and -3 and the Bcl-2 interacting domain (Bid). Collectively, our results showed that EG induces apoptosis in HL-60 via mitochondrial-mediated pathways.

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Effect of ethyl gallate (EG) on the morphology and viability of HL-60 cells. Cells were cultured with 50 μM, 75 μM, 100 μM, 150 μM, 200 μM, or 300 μM EG for 24 h or 48 h. (A) The morphological changes of HL-60 cells were visualized by phase-contrast microscopy (200×); (B) Cell viability was measured by the methanethiosulfonate/phenazine methosulfate solution (MTS) assay. Each point is the mean ± SD of 3 experiments.
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f1-ijms-13-11912: Effect of ethyl gallate (EG) on the morphology and viability of HL-60 cells. Cells were cultured with 50 μM, 75 μM, 100 μM, 150 μM, 200 μM, or 300 μM EG for 24 h or 48 h. (A) The morphological changes of HL-60 cells were visualized by phase-contrast microscopy (200×); (B) Cell viability was measured by the methanethiosulfonate/phenazine methosulfate solution (MTS) assay. Each point is the mean ± SD of 3 experiments.

Mentions: After treatment for 24 h or 48 h with EG, HL-60 cells showed changes in morphology, including shrinkage of the cell membrane and the development of apoptotic bodies (Figure 1A). Consistent with these effects, the viability of EG-treated cells decreased in a time- and dose-dependent manner (Figure 1B), demonstrating that EG has a cytotoxic effect on HL-60 cells.


Ethyl gallate induces apoptosis of HL-60 cells by promoting the expression of caspases-8, -9, -3, apoptosis-inducing factor and endonuclease G.

Kim WH, Song HO, Choi HJ, Bang HI, Choi DY, Park H - Int J Mol Sci (2012)

Effect of ethyl gallate (EG) on the morphology and viability of HL-60 cells. Cells were cultured with 50 μM, 75 μM, 100 μM, 150 μM, 200 μM, or 300 μM EG for 24 h or 48 h. (A) The morphological changes of HL-60 cells were visualized by phase-contrast microscopy (200×); (B) Cell viability was measured by the methanethiosulfonate/phenazine methosulfate solution (MTS) assay. Each point is the mean ± SD of 3 experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3472783&req=5

f1-ijms-13-11912: Effect of ethyl gallate (EG) on the morphology and viability of HL-60 cells. Cells were cultured with 50 μM, 75 μM, 100 μM, 150 μM, 200 μM, or 300 μM EG for 24 h or 48 h. (A) The morphological changes of HL-60 cells were visualized by phase-contrast microscopy (200×); (B) Cell viability was measured by the methanethiosulfonate/phenazine methosulfate solution (MTS) assay. Each point is the mean ± SD of 3 experiments.
Mentions: After treatment for 24 h or 48 h with EG, HL-60 cells showed changes in morphology, including shrinkage of the cell membrane and the development of apoptotic bodies (Figure 1A). Consistent with these effects, the viability of EG-treated cells decreased in a time- and dose-dependent manner (Figure 1B), demonstrating that EG has a cytotoxic effect on HL-60 cells.

Bottom Line: Western blotting analysis indicated that EG-mediated HL-60 apoptosis mainly occurred through the mitochondrial pathway, as shown by the release of cytochrome c, apoptosis-inducing factor (AIF), and endonuclease G (Endo G), as well as the upregulation of Bcl-2-associated X protein (Bax).EG also activated the death receptor-dependent pathway of apoptosis by enhancing the expression of caspases-8, -9, and -3 and the Bcl-2 interacting domain (Bid).Collectively, our results showed that EG induces apoptosis in HL-60 via mitochondrial-mediated pathways.

View Article: PubMed Central - PubMed

Affiliation: Department of Infection Biology, Zoonosis Research Center, Wonkwang University School of Medicine, 344-2, Shinyong-dong, Iksan, Chonbuk 570-749, South Korea; E-Mails: woong621@gmail.com (W.-H.K.); sea5328@daum.net (H.-O.S.); rerived@empal.com (H.-J.C.).

ABSTRACT
Many phytochemicals have been recognized to have potential therapeutic efficacy in cancer treatment. In this study, we investigated ethyl gallate (EG) for possible proapoptotic effects in the human promyelocytic leukemia cell line, HL-60. We examined cell viability, morphological changes, DNA content and fragmentation, and expression of apoptosis-related proteins for up to 48 h after EG treatment. The results showed that EG induced morphological changes and DNA fragmentation and reduced HL-60 cell viability in a dose-dependent and time-dependent manner. Western blotting analysis indicated that EG-mediated HL-60 apoptosis mainly occurred through the mitochondrial pathway, as shown by the release of cytochrome c, apoptosis-inducing factor (AIF), and endonuclease G (Endo G), as well as the upregulation of Bcl-2-associated X protein (Bax). EG also activated the death receptor-dependent pathway of apoptosis by enhancing the expression of caspases-8, -9, and -3 and the Bcl-2 interacting domain (Bid). Collectively, our results showed that EG induces apoptosis in HL-60 via mitochondrial-mediated pathways.

Show MeSH
Related in: MedlinePlus