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Suppression of E-cadherin mediates gallotannin induced apoptosis in Hep G2 hepatocelluar carcinoma cells.

Han HJ, Kwon HY, Sohn EJ, Ko H, Kim B, Jung K, Lew JH, Kim SH - Int. J. Biol. Sci. (2014)

Bottom Line: Consistently, Immunofluorescence assay showed that E-cadherin or β-catenin expression was suppressed in a time dependent manner by gallotannin.Furthermore, silencing of E-cadherin by siRNA transfection method enhanced PAPR cleavage, caspase 3 activation and sub G1 population and attenuated the cell adhesion induced by gallotannin in Hep G2 cells.Overall, our findings demonstrate that the disruption of cell adhesion junction by suppression of E-cadherin mediates gallotannin enhanced apoptosis in Hep G2 liver cancer cells.

View Article: PubMed Central - PubMed

Affiliation: 2. Graduate School of East-West Medical Science, Kyung Hee University, Yongin 449-701, Republic of Korea.

ABSTRACT
Though gallotannin was known to have anti-oxidant and antitumor activity, the underlying antitumor mechanism of gallotannin still remains unclear. Thus, in the present study, antitumor mechanism of gallotannin was elucidated in hepatocellular carcinoma cells. Gallotannin significantly exerted cytotoxicity against Hep G2 and Chang hepatocellular carcinoma cells with the accumulation of the sub-G1 population and increase of terminal deoxynucleotidyltransferasedUTP nick end labeling (TUNEL) positive cells as an apoptotic feature. Also, gallotannin attenuated the expression of pro-caspase9, pro-caspase3, Bcl2 and integrin β1 and cleaved poly(ADP)-ribose polymerase (PARP) in Hep G2 and Chang cancer cells. Furthermore, gallotannin suppressed cell repair motility by wound healing assay and also inhibited cell adhesion in Hep G2 cells. Of note, gallotannin attenuated the expression of epithelial cadherin (E-cadherin) to form cell-cell adhesion from the early stage, and also beta-catenin at late phase in Hep G2 cells. Consistently, Immunofluorescence assay showed that E-cadherin or β-catenin expression was suppressed in a time dependent manner by gallotannin. Furthermore, silencing of E-cadherin by siRNA transfection method enhanced PAPR cleavage, caspase 3 activation and sub G1 population and attenuated the cell adhesion induced by gallotannin in Hep G2 cells. Overall, our findings demonstrate that the disruption of cell adhesion junction by suppression of E-cadherin mediates gallotannin enhanced apoptosis in Hep G2 liver cancer cells.

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Gallotannin exerted the cytotoxicity against Hep G2 and Chang hepatocellular carcinoma cells. (A) Structure of gallotannin. (B) Cytotoxicity of gallotannin in Hep G2. Hep G2 cells were treated with various concentrations of gallotannin (0, 2, 4, 8, or 16 μM) for 48 h and XTT assay was used.to find out cytotoxicity and apoptotic morphological changes in gallotannin treated Hep G2 (C) or Chang (D) cells under inverted microscopy at ×200 magnification.
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Figure 1: Gallotannin exerted the cytotoxicity against Hep G2 and Chang hepatocellular carcinoma cells. (A) Structure of gallotannin. (B) Cytotoxicity of gallotannin in Hep G2. Hep G2 cells were treated with various concentrations of gallotannin (0, 2, 4, 8, or 16 μM) for 48 h and XTT assay was used.to find out cytotoxicity and apoptotic morphological changes in gallotannin treated Hep G2 (C) or Chang (D) cells under inverted microscopy at ×200 magnification.

Mentions: Gallotannin (Figure 1A) was purchased from Sigma-Aldrich (Sigma-Aldrich, St.Louis, MO, U.S.A.).


Suppression of E-cadherin mediates gallotannin induced apoptosis in Hep G2 hepatocelluar carcinoma cells.

Han HJ, Kwon HY, Sohn EJ, Ko H, Kim B, Jung K, Lew JH, Kim SH - Int. J. Biol. Sci. (2014)

Gallotannin exerted the cytotoxicity against Hep G2 and Chang hepatocellular carcinoma cells. (A) Structure of gallotannin. (B) Cytotoxicity of gallotannin in Hep G2. Hep G2 cells were treated with various concentrations of gallotannin (0, 2, 4, 8, or 16 μM) for 48 h and XTT assay was used.to find out cytotoxicity and apoptotic morphological changes in gallotannin treated Hep G2 (C) or Chang (D) cells under inverted microscopy at ×200 magnification.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4007362&req=5

Figure 1: Gallotannin exerted the cytotoxicity against Hep G2 and Chang hepatocellular carcinoma cells. (A) Structure of gallotannin. (B) Cytotoxicity of gallotannin in Hep G2. Hep G2 cells were treated with various concentrations of gallotannin (0, 2, 4, 8, or 16 μM) for 48 h and XTT assay was used.to find out cytotoxicity and apoptotic morphological changes in gallotannin treated Hep G2 (C) or Chang (D) cells under inverted microscopy at ×200 magnification.
Mentions: Gallotannin (Figure 1A) was purchased from Sigma-Aldrich (Sigma-Aldrich, St.Louis, MO, U.S.A.).

Bottom Line: Consistently, Immunofluorescence assay showed that E-cadherin or β-catenin expression was suppressed in a time dependent manner by gallotannin.Furthermore, silencing of E-cadherin by siRNA transfection method enhanced PAPR cleavage, caspase 3 activation and sub G1 population and attenuated the cell adhesion induced by gallotannin in Hep G2 cells.Overall, our findings demonstrate that the disruption of cell adhesion junction by suppression of E-cadherin mediates gallotannin enhanced apoptosis in Hep G2 liver cancer cells.

View Article: PubMed Central - PubMed

Affiliation: 2. Graduate School of East-West Medical Science, Kyung Hee University, Yongin 449-701, Republic of Korea.

ABSTRACT
Though gallotannin was known to have anti-oxidant and antitumor activity, the underlying antitumor mechanism of gallotannin still remains unclear. Thus, in the present study, antitumor mechanism of gallotannin was elucidated in hepatocellular carcinoma cells. Gallotannin significantly exerted cytotoxicity against Hep G2 and Chang hepatocellular carcinoma cells with the accumulation of the sub-G1 population and increase of terminal deoxynucleotidyltransferasedUTP nick end labeling (TUNEL) positive cells as an apoptotic feature. Also, gallotannin attenuated the expression of pro-caspase9, pro-caspase3, Bcl2 and integrin β1 and cleaved poly(ADP)-ribose polymerase (PARP) in Hep G2 and Chang cancer cells. Furthermore, gallotannin suppressed cell repair motility by wound healing assay and also inhibited cell adhesion in Hep G2 cells. Of note, gallotannin attenuated the expression of epithelial cadherin (E-cadherin) to form cell-cell adhesion from the early stage, and also beta-catenin at late phase in Hep G2 cells. Consistently, Immunofluorescence assay showed that E-cadherin or β-catenin expression was suppressed in a time dependent manner by gallotannin. Furthermore, silencing of E-cadherin by siRNA transfection method enhanced PAPR cleavage, caspase 3 activation and sub G1 population and attenuated the cell adhesion induced by gallotannin in Hep G2 cells. Overall, our findings demonstrate that the disruption of cell adhesion junction by suppression of E-cadherin mediates gallotannin enhanced apoptosis in Hep G2 liver cancer cells.

Show MeSH
Related in: MedlinePlus