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Ursolic acid inhibits proliferation and induces apoptosis of cancer cells in vitro and in vivo.

Wang X, Zhang F, Yang L, Mei Y, Long H, Zhang X, Zhang J - J. Biomed. Biotechnol. (2011)

Bottom Line: UA inhibits growth of BGC-803 cells in vitro in dose-dependent and time-dependent manner.DNA fragmentation was found in BGC-803 cells exposed to UA.UA activated caspase-3, -8, and -9 and down regulated expression of Bcl-2 in BGC-803 cells.

View Article: PubMed Central - PubMed

Affiliation: PET-CT Center, The Affiliated Hospital of Inner Mongolia Medical College, TongDao North Street, Hohhot 010050, China.

ABSTRACT
The aims of the study are to explore the effect of ursolic acid (UA) on the growth of gastric cancer cell line BGC-803 and hepatocellular cancer cell H22 xenograft and to understand the mechanism. UA inhibits growth of BGC-803 cells in vitro in dose-dependent and time-dependent manner. Treated with UA in vivo, tumor cells can be arrested to G0/G1 stage. The apoptotic rate was significantly increased in tumor cells treated with UA both in vitro and in vivo. DNA fragmentation was found in BGC-803 cells exposed to UA. UA activated caspase-3, -8, and -9 and down regulated expression of Bcl-2 in BGC-803 cells. The expression of caspase-3 and -8 was elevated in tumor cells from xenograft treated with UA. ¹⁸F-FLT PET-CT imaging confirmed tumor model and UA effectiveness. Our results indicated that UA inhibits growth of tumor cells both in vitro and in vivo by decreasing proliferation of cells and inducing apoptosis.

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UA inhibited proliferation and induced apoptosis in hepatocellular carcinoma cell H22 mouse xenograft. (a) Xenografts treated with PS or UA were imaged by PET-CT. (b) Cell cycle of tumor cells from xenografts treated with PS or UA was examined. Cell cycle distribution was showed in the table (*P < .05). (c) Apoptosis of tumor cells from xenografts induced by UA was detected by Annexin-V staining and flow cytometry. Quantified data showed in the table below (*P < .05). (d) Western blot showed expression of Caspase-3 and Caspase-8 in tumor cells from xenografts treated with PS or UA.
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fig2: UA inhibited proliferation and induced apoptosis in hepatocellular carcinoma cell H22 mouse xenograft. (a) Xenografts treated with PS or UA were imaged by PET-CT. (b) Cell cycle of tumor cells from xenografts treated with PS or UA was examined. Cell cycle distribution was showed in the table (*P < .05). (c) Apoptosis of tumor cells from xenografts induced by UA was detected by Annexin-V staining and flow cytometry. Quantified data showed in the table below (*P < .05). (d) Western blot showed expression of Caspase-3 and Caspase-8 in tumor cells from xenografts treated with PS or UA.

Mentions: Compared to negative control, xenografts which were treated with UA were robust and had more weight (Table 2). There was 52.8% inhibition rate of tumor growth in UA treatment xenografts. Tumor tissue was examined under optical microscope after H&E staining. Tumor cells in negative control resembled nests or cords and showed vigorous mitosis. Nuclei of tumor cells were round or oval; while there was more necrosis and apoptosis in UA treatment group, density of tumor cells decreased. We examined the proliferation of tumor cells in xenografts by PET-CT. Xenografts was injected with 18F-FLT, and the whole mouse was imaged by PET-CT. Focal 18F-FLT uptake could be observed in tumor and abdominal cavity in xenografts of PS control (Figure 2(a) upper panel). Xenografts with UA treatment showed lower 18F-FLT uptake in tumor (Figure 2(a) lower panel). The image of PET-CT showed directly that proliferation of tumor cells declined by UA treatment in vivo. To elucidate the mechanism how UA inhibited proliferation of tumor cells, we examined cell cycle of these tumor cells in xenografts. Percentange of 38.71 ± 3.27 of the tumor cells treated with UA were in G0/G1 stage (P < .05, Figure 2(b)), but 48.97 ± 3.96% and 23.53 ± 5.97% cells were in S or G2/M stage for the negative control, suggesting that UA treatment decreased proliferation of tumor cells in mouse xenograft model.


Ursolic acid inhibits proliferation and induces apoptosis of cancer cells in vitro and in vivo.

Wang X, Zhang F, Yang L, Mei Y, Long H, Zhang X, Zhang J - J. Biomed. Biotechnol. (2011)

UA inhibited proliferation and induced apoptosis in hepatocellular carcinoma cell H22 mouse xenograft. (a) Xenografts treated with PS or UA were imaged by PET-CT. (b) Cell cycle of tumor cells from xenografts treated with PS or UA was examined. Cell cycle distribution was showed in the table (*P < .05). (c) Apoptosis of tumor cells from xenografts induced by UA was detected by Annexin-V staining and flow cytometry. Quantified data showed in the table below (*P < .05). (d) Western blot showed expression of Caspase-3 and Caspase-8 in tumor cells from xenografts treated with PS or UA.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3116524&req=5

fig2: UA inhibited proliferation and induced apoptosis in hepatocellular carcinoma cell H22 mouse xenograft. (a) Xenografts treated with PS or UA were imaged by PET-CT. (b) Cell cycle of tumor cells from xenografts treated with PS or UA was examined. Cell cycle distribution was showed in the table (*P < .05). (c) Apoptosis of tumor cells from xenografts induced by UA was detected by Annexin-V staining and flow cytometry. Quantified data showed in the table below (*P < .05). (d) Western blot showed expression of Caspase-3 and Caspase-8 in tumor cells from xenografts treated with PS or UA.
Mentions: Compared to negative control, xenografts which were treated with UA were robust and had more weight (Table 2). There was 52.8% inhibition rate of tumor growth in UA treatment xenografts. Tumor tissue was examined under optical microscope after H&E staining. Tumor cells in negative control resembled nests or cords and showed vigorous mitosis. Nuclei of tumor cells were round or oval; while there was more necrosis and apoptosis in UA treatment group, density of tumor cells decreased. We examined the proliferation of tumor cells in xenografts by PET-CT. Xenografts was injected with 18F-FLT, and the whole mouse was imaged by PET-CT. Focal 18F-FLT uptake could be observed in tumor and abdominal cavity in xenografts of PS control (Figure 2(a) upper panel). Xenografts with UA treatment showed lower 18F-FLT uptake in tumor (Figure 2(a) lower panel). The image of PET-CT showed directly that proliferation of tumor cells declined by UA treatment in vivo. To elucidate the mechanism how UA inhibited proliferation of tumor cells, we examined cell cycle of these tumor cells in xenografts. Percentange of 38.71 ± 3.27 of the tumor cells treated with UA were in G0/G1 stage (P < .05, Figure 2(b)), but 48.97 ± 3.96% and 23.53 ± 5.97% cells were in S or G2/M stage for the negative control, suggesting that UA treatment decreased proliferation of tumor cells in mouse xenograft model.

Bottom Line: UA inhibits growth of BGC-803 cells in vitro in dose-dependent and time-dependent manner.DNA fragmentation was found in BGC-803 cells exposed to UA.UA activated caspase-3, -8, and -9 and down regulated expression of Bcl-2 in BGC-803 cells.

View Article: PubMed Central - PubMed

Affiliation: PET-CT Center, The Affiliated Hospital of Inner Mongolia Medical College, TongDao North Street, Hohhot 010050, China.

ABSTRACT
The aims of the study are to explore the effect of ursolic acid (UA) on the growth of gastric cancer cell line BGC-803 and hepatocellular cancer cell H22 xenograft and to understand the mechanism. UA inhibits growth of BGC-803 cells in vitro in dose-dependent and time-dependent manner. Treated with UA in vivo, tumor cells can be arrested to G0/G1 stage. The apoptotic rate was significantly increased in tumor cells treated with UA both in vitro and in vivo. DNA fragmentation was found in BGC-803 cells exposed to UA. UA activated caspase-3, -8, and -9 and down regulated expression of Bcl-2 in BGC-803 cells. The expression of caspase-3 and -8 was elevated in tumor cells from xenograft treated with UA. ¹⁸F-FLT PET-CT imaging confirmed tumor model and UA effectiveness. Our results indicated that UA inhibits growth of tumor cells both in vitro and in vivo by decreasing proliferation of cells and inducing apoptosis.

Show MeSH
Related in: MedlinePlus