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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 gastric cancer cell BGC-803. (a) Inhibition of proliferation of BGC-803 was assessed by MMT staining. (b) Morphological changes of BGC-803 cells after UA (IC50  (24 h)) treatment for 24 h (Bar represents 200 μm); magnified image of cells was showed in corner (Bar represents 200 μm). (c) H&E staining of BGC-803 cells after UA (IC50  (24 h)) treatment for 24 h (Bar represents 200 μm), and arrows indicated apoptotic cells; magnified image of cells was showed in corner (Bar represents 200 μm). (d) DNA ladder was found in BGC-803 cells treated with UA (IC50  (24 h) and IC50  (36 h)), not in BGC-803 cells treated with 0.2% DMSO or without treatment. (e) Apoptosis of BGC-803 cells induced by UA was detected by Annexin-V staining and flow cytometry. (f) was the quantified data from experiment showed in (e). Apoptotic rate was 0.66 ± 0.15, 0.67 ± 0.08, and 1.69 ± 0.11 in control, DMSO, and UA treated cells, respectively, (*P < .01). (g) Western blot showed expression of apoptotic related genes in BGC-803 cell treated with DMSO, UA and without treatment; β-actin was used as internal control. (h) showed related amount of protein from (g) (*P < .05).
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fig1: UA inhibited proliferation and induced apoptosis in gastric cancer cell BGC-803. (a) Inhibition of proliferation of BGC-803 was assessed by MMT staining. (b) Morphological changes of BGC-803 cells after UA (IC50 (24 h)) treatment for 24 h (Bar represents 200 μm); magnified image of cells was showed in corner (Bar represents 200 μm). (c) H&E staining of BGC-803 cells after UA (IC50 (24 h)) treatment for 24 h (Bar represents 200 μm), and arrows indicated apoptotic cells; magnified image of cells was showed in corner (Bar represents 200 μm). (d) DNA ladder was found in BGC-803 cells treated with UA (IC50 (24 h) and IC50 (36 h)), not in BGC-803 cells treated with 0.2% DMSO or without treatment. (e) Apoptosis of BGC-803 cells induced by UA was detected by Annexin-V staining and flow cytometry. (f) was the quantified data from experiment showed in (e). Apoptotic rate was 0.66 ± 0.15, 0.67 ± 0.08, and 1.69 ± 0.11 in control, DMSO, and UA treated cells, respectively, (*P < .01). (g) Western blot showed expression of apoptotic related genes in BGC-803 cell treated with DMSO, UA and without treatment; β-actin was used as internal control. (h) showed related amount of protein from (g) (*P < .05).

Mentions: Proliferation of BGC-803 cells was examined to assess whether UA had inhibitory effect on BGC-803. Cells were treated with different concentrations of UA (10, 20, 30, 40, 50, 60 μmol/L) for 12, 24, 36, 48 h, respectively. Compared with control, UA (20–60 μmol/L) inhibited BGC-803 cell proliferation in dose- and time-dependent manners. However, 10 μmol/L of UA did not show inhibitory effect (Figure 1(a)). The IC50 of UA at different time points (12 h, 24 h, 36 h and 48 h) were 61.29 μM, 43.78 μM, 35.94 μM, and 24.95 μM, respectively (Table 1).


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 gastric cancer cell BGC-803. (a) Inhibition of proliferation of BGC-803 was assessed by MMT staining. (b) Morphological changes of BGC-803 cells after UA (IC50  (24 h)) treatment for 24 h (Bar represents 200 μm); magnified image of cells was showed in corner (Bar represents 200 μm). (c) H&E staining of BGC-803 cells after UA (IC50  (24 h)) treatment for 24 h (Bar represents 200 μm), and arrows indicated apoptotic cells; magnified image of cells was showed in corner (Bar represents 200 μm). (d) DNA ladder was found in BGC-803 cells treated with UA (IC50  (24 h) and IC50  (36 h)), not in BGC-803 cells treated with 0.2% DMSO or without treatment. (e) Apoptosis of BGC-803 cells induced by UA was detected by Annexin-V staining and flow cytometry. (f) was the quantified data from experiment showed in (e). Apoptotic rate was 0.66 ± 0.15, 0.67 ± 0.08, and 1.69 ± 0.11 in control, DMSO, and UA treated cells, respectively, (*P < .01). (g) Western blot showed expression of apoptotic related genes in BGC-803 cell treated with DMSO, UA and without treatment; β-actin was used as internal control. (h) showed related amount of protein from (g) (*P < .05).
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3116524&req=5

fig1: UA inhibited proliferation and induced apoptosis in gastric cancer cell BGC-803. (a) Inhibition of proliferation of BGC-803 was assessed by MMT staining. (b) Morphological changes of BGC-803 cells after UA (IC50 (24 h)) treatment for 24 h (Bar represents 200 μm); magnified image of cells was showed in corner (Bar represents 200 μm). (c) H&E staining of BGC-803 cells after UA (IC50 (24 h)) treatment for 24 h (Bar represents 200 μm), and arrows indicated apoptotic cells; magnified image of cells was showed in corner (Bar represents 200 μm). (d) DNA ladder was found in BGC-803 cells treated with UA (IC50 (24 h) and IC50 (36 h)), not in BGC-803 cells treated with 0.2% DMSO or without treatment. (e) Apoptosis of BGC-803 cells induced by UA was detected by Annexin-V staining and flow cytometry. (f) was the quantified data from experiment showed in (e). Apoptotic rate was 0.66 ± 0.15, 0.67 ± 0.08, and 1.69 ± 0.11 in control, DMSO, and UA treated cells, respectively, (*P < .01). (g) Western blot showed expression of apoptotic related genes in BGC-803 cell treated with DMSO, UA and without treatment; β-actin was used as internal control. (h) showed related amount of protein from (g) (*P < .05).
Mentions: Proliferation of BGC-803 cells was examined to assess whether UA had inhibitory effect on BGC-803. Cells were treated with different concentrations of UA (10, 20, 30, 40, 50, 60 μmol/L) for 12, 24, 36, 48 h, respectively. Compared with control, UA (20–60 μmol/L) inhibited BGC-803 cell proliferation in dose- and time-dependent manners. However, 10 μmol/L of UA did not show inhibitory effect (Figure 1(a)). The IC50 of UA at different time points (12 h, 24 h, 36 h and 48 h) were 61.29 μM, 43.78 μM, 35.94 μM, and 24.95 μM, respectively (Table 1).

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