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Anti-tumor activity of a novel protein obtained from tartary buckwheat.

Guo X, Zhu K, Zhang H, Yao H - Int J Mol Sci (2010)

Bottom Line: Cell-cycle analysis revealed that treatment with TBWSP31 resulted in a G(0)/G(1) arrest and prevented the cells from growing from G(0)/G(1) phase to S phase, which was most prominent at 48 h.The expression of bcl-2 and Fas were detected quantitatively by FCM, which showed that TBWSP31 induced-apoptosis may be involved with the participation of Fas and bcl-2.These results suggest that TBWSP31 is a potential antitumor compound and that apoptosis induced by TBWSP31 is a key antitumor mechanism.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Food Science and Technology, Jiangnan University, 1800 Lihu Road, Wuxi-214122, Jiangsu, China; E-Mails: zkx1978@hotmail.com (K.Z.); hui1003@hotmail.com (H.Z.); hyyao@jiangnan.edu.cn (H.Y.).

ABSTRACT
TBWSP31 is a novel antitumor protein that was isolated from tartary buckwheat water-soluble extracts. The objective of this paper was to investigate the anti-proliferative effects of TBWSP31 on breast cancer Bcap37cells and to explore its possible mechanism. After treatment of Bcap37 cells with TBWSP31, typical apoptotic morphological changes were observed by inverted microscopy and scanning electron microscopy (SEM), such as detachment from the culture plate, change to a round shape, cell shrinkage, the absence of obvious microvilli, plasma membrane blebbing, and formation of apoptotic bodies. Cell-cycle analysis revealed that treatment with TBWSP31 resulted in a G(0)/G(1) arrest and prevented the cells from growing from G(0)/G(1) phase to S phase, which was most prominent at 48 h. The expression of bcl-2 and Fas were detected quantitatively by FCM, which showed that TBWSP31 induced-apoptosis may be involved with the participation of Fas and bcl-2. These results suggest that TBWSP31 is a potential antitumor compound and that apoptosis induced by TBWSP31 is a key antitumor mechanism.

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The alteration of bcl-2 (A) and Fas (B) protein levels of Bcap37 cells after treatment with TBWSP31, as determined by flow cytometry. Bcap37 cells were treated with 0 (control; left panels), 5 (middle panels) and 10 μg/mL (right panels) of TBWSP31 for 48 h. The percentage of the Bcl-2 and Fas protein are shown at the top right of each panel.
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f4-ijms-11-05201: The alteration of bcl-2 (A) and Fas (B) protein levels of Bcap37 cells after treatment with TBWSP31, as determined by flow cytometry. Bcap37 cells were treated with 0 (control; left panels), 5 (middle panels) and 10 μg/mL (right panels) of TBWSP31 for 48 h. The percentage of the Bcl-2 and Fas protein are shown at the top right of each panel.

Mentions: The effect of TBWSP31 on the levels of bcl-2 and Fas proteins in Bcap37 cells is shown in Figure 4. The level of bcl-2 decreased dramatically from 71.5% (0 μg/mL, control) to 46.7% and 32.3% when Bcap37 cells were treated with 5 μg/mL and 10 μg/mL of TBWSP31, respectively (p < 0.01) (see Figure 4A). In contrast, the levels of Fas protein increased significantly after TBWSP31 treatment: from 2.83% (0 μg/mL, control) to 13.3% (5 μg/mL) and 27.0% (10 μg/mL) (p < 0.01) (Figure 4B). These results showed that TBWSP31 treatment induced a significant decrease of bcl-2 expression and increase of Fas expression after 48 h in a dose-dependent manner. Cell apoptosis is regulated by anti-apoptotic and pro-apoptotic effectors, involving a large number of biomolecules. Bcl-2 is known to be an upstream effector molecule in the apoptotic pathway and is identified as a potent suppressor of apoptosis [26]. Fas protein, a glycosylated 45-kD transmembrane receptor, belongs to the tumor necrosis factor receptor family and induces apoptosis [27]. In the present study, the expression of bcl-2 was down-regulated and the expression of Fas was up-regulated. The changes of these proteins-correlated apoptosis expressions suggested that TBWSP31 induced-apoptosis may be involved with the participation of Fas and Bcl-2.


Anti-tumor activity of a novel protein obtained from tartary buckwheat.

Guo X, Zhu K, Zhang H, Yao H - Int J Mol Sci (2010)

The alteration of bcl-2 (A) and Fas (B) protein levels of Bcap37 cells after treatment with TBWSP31, as determined by flow cytometry. Bcap37 cells were treated with 0 (control; left panels), 5 (middle panels) and 10 μg/mL (right panels) of TBWSP31 for 48 h. The percentage of the Bcl-2 and Fas protein are shown at the top right of each panel.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3100852&req=5

f4-ijms-11-05201: The alteration of bcl-2 (A) and Fas (B) protein levels of Bcap37 cells after treatment with TBWSP31, as determined by flow cytometry. Bcap37 cells were treated with 0 (control; left panels), 5 (middle panels) and 10 μg/mL (right panels) of TBWSP31 for 48 h. The percentage of the Bcl-2 and Fas protein are shown at the top right of each panel.
Mentions: The effect of TBWSP31 on the levels of bcl-2 and Fas proteins in Bcap37 cells is shown in Figure 4. The level of bcl-2 decreased dramatically from 71.5% (0 μg/mL, control) to 46.7% and 32.3% when Bcap37 cells were treated with 5 μg/mL and 10 μg/mL of TBWSP31, respectively (p < 0.01) (see Figure 4A). In contrast, the levels of Fas protein increased significantly after TBWSP31 treatment: from 2.83% (0 μg/mL, control) to 13.3% (5 μg/mL) and 27.0% (10 μg/mL) (p < 0.01) (Figure 4B). These results showed that TBWSP31 treatment induced a significant decrease of bcl-2 expression and increase of Fas expression after 48 h in a dose-dependent manner. Cell apoptosis is regulated by anti-apoptotic and pro-apoptotic effectors, involving a large number of biomolecules. Bcl-2 is known to be an upstream effector molecule in the apoptotic pathway and is identified as a potent suppressor of apoptosis [26]. Fas protein, a glycosylated 45-kD transmembrane receptor, belongs to the tumor necrosis factor receptor family and induces apoptosis [27]. In the present study, the expression of bcl-2 was down-regulated and the expression of Fas was up-regulated. The changes of these proteins-correlated apoptosis expressions suggested that TBWSP31 induced-apoptosis may be involved with the participation of Fas and Bcl-2.

Bottom Line: Cell-cycle analysis revealed that treatment with TBWSP31 resulted in a G(0)/G(1) arrest and prevented the cells from growing from G(0)/G(1) phase to S phase, which was most prominent at 48 h.The expression of bcl-2 and Fas were detected quantitatively by FCM, which showed that TBWSP31 induced-apoptosis may be involved with the participation of Fas and bcl-2.These results suggest that TBWSP31 is a potential antitumor compound and that apoptosis induced by TBWSP31 is a key antitumor mechanism.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Food Science and Technology, Jiangnan University, 1800 Lihu Road, Wuxi-214122, Jiangsu, China; E-Mails: zkx1978@hotmail.com (K.Z.); hui1003@hotmail.com (H.Z.); hyyao@jiangnan.edu.cn (H.Y.).

ABSTRACT
TBWSP31 is a novel antitumor protein that was isolated from tartary buckwheat water-soluble extracts. The objective of this paper was to investigate the anti-proliferative effects of TBWSP31 on breast cancer Bcap37cells and to explore its possible mechanism. After treatment of Bcap37 cells with TBWSP31, typical apoptotic morphological changes were observed by inverted microscopy and scanning electron microscopy (SEM), such as detachment from the culture plate, change to a round shape, cell shrinkage, the absence of obvious microvilli, plasma membrane blebbing, and formation of apoptotic bodies. Cell-cycle analysis revealed that treatment with TBWSP31 resulted in a G(0)/G(1) arrest and prevented the cells from growing from G(0)/G(1) phase to S phase, which was most prominent at 48 h. The expression of bcl-2 and Fas were detected quantitatively by FCM, which showed that TBWSP31 induced-apoptosis may be involved with the participation of Fas and bcl-2. These results suggest that TBWSP31 is a potential antitumor compound and that apoptosis induced by TBWSP31 is a key antitumor mechanism.

Show MeSH
Related in: MedlinePlus