In this study, we evaluated the anti-cancer property of five bark extracts and the isolates from chloroform and ethyl acetate of Annickia chlorantha by the tetrazolium salt method (MTT method). The anti-cancer activit...In this study, we evaluated the anti-cancer property of five bark extracts and the isolates from chloroform and ethyl acetate of Annickia chlorantha by the tetrazolium salt method (MTT method). The anti-cancer activity was performed on human prostate cancer cell lines PC-3 and hormone-dependent breast cancer cell lines MCF-7. Results indicated that the two isolates displayed interesting cytotoxicity towards MCF-7 cell lines with CC<sub>50</sub> of 3.84 CC<sub>50</sub>/mL and 4.87 CC<sub>50</sub>/mL for chloroform and ethyl acetate respectively;while the total bark extracts showed CC<sub>50</sub> of 24.33 CC<sub>50</sub>/mL, 36.49 CC<sub>50</sub>/ mL and 73.52 CC<sub>50</sub>/mL for chloroform, ethyl acetate and methanol extracts respectively. By the other hand on PC-3, the CC<sub>50</sub> of the isolates were higher than the one on MCF-7, more than 10 CC<sub>50</sub>/mL for both chloroform and ethyl acetate isolates and 49.14 CC<sub>50</sub>/mL, 77.33 CC<sub>50</sub>/mL, 89.38 CC<sub>50</sub>/mL and 92.37 CC<sub>50</sub>/mL, respectively for chloroform, ethyl acetate and methanol soluble extracts. From this study, we identified that the two isolates had anti-cancer properties against MCF-7 cell lines.展开更多
Aim: To investigate the possible role of manganese in the regulation of mitochondrial aconitase (mACON) activity human prostate carcinoma cell line PC-3 cells. Methods: The mACON enzymatic activities of human pros...Aim: To investigate the possible role of manganese in the regulation of mitochondrial aconitase (mACON) activity human prostate carcinoma cell line PC-3 cells. Methods: The mACON enzymatic activities of human prostate carcinoma cell line PC-3 cells were determined using a reduced nicotinamide adenine dinucleotide-coupled assay. Immunoblot and transient gene expression assays were used to study gene expression of the mACON. The putative response element for gene expression was identified using reporter assays with site-directed mutagenesis and electrophoretic mobility-shift assays. Results: In vitro study revealed that manganese chloride (MnCI2) treatment for 16 h inhibited the enzymatic activity of mACON, which induced the inhibition of citrate utility and cell proliferation of PC- 3 cells. Although results from transient gene expression assays showed that MnCI2 treatment upregulated gene translation by approximately 5-fold through the iron response element pathway, immunoblot and reporter assays showed that MnCl2 treatments inhibited protein and gene expression of mACON. This effect was reversed by cotreatment with ferric ammonium citrate. Additional reporter assays with site-directed mutagenesis and electrophoretic mobility-shift assays suggested that a putative metal response element in the promoter of the mACON gene was involved in the regulation of MnCh on the gene expression of mACON. Conclusion: These findings suggest that manganese acts as an antagonist of iron, disrupting the enzymatic activity and gene expression of mACON and citrate metabolism in the prostate.展开更多
Aim:To investigate the possible role of manganese in the regulation of mitochondrial aconitase(mACON)activity human prostate carcinoma cell line PC-3 cells.Methods:The mACON enzymatic activities of human prostate carc...Aim:To investigate the possible role of manganese in the regulation of mitochondrial aconitase(mACON)activity human prostate carcinoma cell line PC-3 cells.Methods:The mACON enzymatic activities of human prostate carcinoma cell line PC-3 cells were determined using a reduced nicotinamide adenine dmucleotide-coupled assay. Immunoblot and transient gene expression assays were used to study gene expression of the mACON.The putative response element for gene expression was identified using reporter assays with site-directed mutagenesis and electro- phoretic mobility-shift assays.Results:In vitro study revealed that manganese chloride(MnCl2)treatment for 16h inhibited the enzymatic activity of mACON,which induced the inhibition of citrate utility and cell proliferation of PC- 3 cells.Although results from transient gene expression assays showed that MnCl_2,treatment upregulated gene translation by approximately 5-fold through the iron response element pathway,immunoblot and reporter assays showed that MnCl_2 treatments inhibited protein and gene expression of mACON.This effect was reversed by co- treatment with fenic ammonium citrate.Additional reporter assays with site-directed mutagenesis and electrophoretic mobility-shift assays suggested that a putative metal response element in the promoter of the mACON gene was involved in the regulation of MnCl_2 on the gene expression of mACON.Conclusion:These findings suggest that manganese acts as an antagonist of iron,disrupting the enzymatic activity and gene expression of mACON and citrate metabolism in the prostate.展开更多
文摘In this study, we evaluated the anti-cancer property of five bark extracts and the isolates from chloroform and ethyl acetate of Annickia chlorantha by the tetrazolium salt method (MTT method). The anti-cancer activity was performed on human prostate cancer cell lines PC-3 and hormone-dependent breast cancer cell lines MCF-7. Results indicated that the two isolates displayed interesting cytotoxicity towards MCF-7 cell lines with CC<sub>50</sub> of 3.84 CC<sub>50</sub>/mL and 4.87 CC<sub>50</sub>/mL for chloroform and ethyl acetate respectively;while the total bark extracts showed CC<sub>50</sub> of 24.33 CC<sub>50</sub>/mL, 36.49 CC<sub>50</sub>/ mL and 73.52 CC<sub>50</sub>/mL for chloroform, ethyl acetate and methanol extracts respectively. By the other hand on PC-3, the CC<sub>50</sub> of the isolates were higher than the one on MCF-7, more than 10 CC<sub>50</sub>/mL for both chloroform and ethyl acetate isolates and 49.14 CC<sub>50</sub>/mL, 77.33 CC<sub>50</sub>/mL, 89.38 CC<sub>50</sub>/mL and 92.37 CC<sub>50</sub>/mL, respectively for chloroform, ethyl acetate and methanol soluble extracts. From this study, we identified that the two isolates had anti-cancer properties against MCF-7 cell lines.
文摘Aim: To investigate the possible role of manganese in the regulation of mitochondrial aconitase (mACON) activity human prostate carcinoma cell line PC-3 cells. Methods: The mACON enzymatic activities of human prostate carcinoma cell line PC-3 cells were determined using a reduced nicotinamide adenine dinucleotide-coupled assay. Immunoblot and transient gene expression assays were used to study gene expression of the mACON. The putative response element for gene expression was identified using reporter assays with site-directed mutagenesis and electrophoretic mobility-shift assays. Results: In vitro study revealed that manganese chloride (MnCI2) treatment for 16 h inhibited the enzymatic activity of mACON, which induced the inhibition of citrate utility and cell proliferation of PC- 3 cells. Although results from transient gene expression assays showed that MnCI2 treatment upregulated gene translation by approximately 5-fold through the iron response element pathway, immunoblot and reporter assays showed that MnCl2 treatments inhibited protein and gene expression of mACON. This effect was reversed by cotreatment with ferric ammonium citrate. Additional reporter assays with site-directed mutagenesis and electrophoretic mobility-shift assays suggested that a putative metal response element in the promoter of the mACON gene was involved in the regulation of MnCh on the gene expression of mACON. Conclusion: These findings suggest that manganese acts as an antagonist of iron, disrupting the enzymatic activity and gene expression of mACON and citrate metabolism in the prostate.
文摘Aim:To investigate the possible role of manganese in the regulation of mitochondrial aconitase(mACON)activity human prostate carcinoma cell line PC-3 cells.Methods:The mACON enzymatic activities of human prostate carcinoma cell line PC-3 cells were determined using a reduced nicotinamide adenine dmucleotide-coupled assay. Immunoblot and transient gene expression assays were used to study gene expression of the mACON.The putative response element for gene expression was identified using reporter assays with site-directed mutagenesis and electro- phoretic mobility-shift assays.Results:In vitro study revealed that manganese chloride(MnCl2)treatment for 16h inhibited the enzymatic activity of mACON,which induced the inhibition of citrate utility and cell proliferation of PC- 3 cells.Although results from transient gene expression assays showed that MnCl_2,treatment upregulated gene translation by approximately 5-fold through the iron response element pathway,immunoblot and reporter assays showed that MnCl_2 treatments inhibited protein and gene expression of mACON.This effect was reversed by co- treatment with fenic ammonium citrate.Additional reporter assays with site-directed mutagenesis and electrophoretic mobility-shift assays suggested that a putative metal response element in the promoter of the mACON gene was involved in the regulation of MnCl_2 on the gene expression of mACON.Conclusion:These findings suggest that manganese acts as an antagonist of iron,disrupting the enzymatic activity and gene expression of mACON and citrate metabolism in the prostate.