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Benzene-poly-carboxylic acid complex, a novel anti-cancer agent induces apoptosis in human breast cancer cells.

Fares F, Azzam N, Fares B, Larsen S, Lindkaer-Jensen S - PLoS ONE (2014)

Bottom Line: Caspases were detected by western blot analysis and gene expression was measured by using the Applied Biosystems® TaqMan® Array Plates.The results showed that exposure of the cells to BP-C1 for 48 h, significantly (P<0.001) reduced cell viability, induced apoptosis and activated caspase 8 and caspace 9.Moreover, gene expression experiments indicated that BP-C1 increased the expression of pro-apoptotic genes (CASP8AP1, TNFRSF21, NFkB2, FADD, BCL10 and CASP8) and lowered the level of mRNA transcripts of inhibitory apoptotic genes (BCL2L11, BCL2L2 and XIAP.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Biology, Faculty of Natural Sciences, University of Haifa, and Department of Molecular Genetics, Carmel Medical Center, Haifa, Israel.

ABSTRACT
Some cases of breast cancer are composed of clones of hormonal-independent growing cells, which do not respond to therapy. In the present study, the effect of Benzene-Poly-Carboxylic Acid Complex (BP-C1) on growth of human breast-cancer cells was tested. BP-C1 is a novel anti-cancer complex of benzene-poly-carboxylic acids with a very low concentration of cis-diammineplatinum (II) dichloride. Human breast cancer cells, MCF-7 and T47D, were used. Cell viability was detected by XTT assay and apoptosis was detected by Flow Cytometry and by annexin V/FITC/PI assay. Caspases were detected by western blot analysis and gene expression was measured by using the Applied Biosystems® TaqMan® Array Plates. The results showed that exposure of the cells to BP-C1 for 48 h, significantly (P<0.001) reduced cell viability, induced apoptosis and activated caspase 8 and caspace 9. Moreover, gene expression experiments indicated that BP-C1 increased the expression of pro-apoptotic genes (CASP8AP1, TNFRSF21, NFkB2, FADD, BCL10 and CASP8) and lowered the level of mRNA transcripts of inhibitory apoptotic genes (BCL2L11, BCL2L2 and XIAP. These findings may lead to the development of new therapeutic strategies for treatment of human cancer using BP-C1 analog.

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Activation of caspase 8 (A) and caspase 9 (C) by BP-C1.Cells were treated with or without 750/ml of BP-C1 for 48 h. Cells were harvested and lysed. Activation of caspase-9 was determined by Western blotting as described under “Materials of Methods”. TA represents paclitaxel and 32c refers to Lx2-32c. Columns represent the densitometry analysis of the indicated proteins. The level of actin in the cells is represented in B and D.
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pone-0085156-g005: Activation of caspase 8 (A) and caspase 9 (C) by BP-C1.Cells were treated with or without 750/ml of BP-C1 for 48 h. Cells were harvested and lysed. Activation of caspase-9 was determined by Western blotting as described under “Materials of Methods”. TA represents paclitaxel and 32c refers to Lx2-32c. Columns represent the densitometry analysis of the indicated proteins. The level of actin in the cells is represented in B and D.

Mentions: To further investigate the mechanistic action of cell death induced by BP-C1, a western blot analysis was performed to detect proteins that have been shown to be involved in both the extrinsic (caspase 8) and intrinsic (caspase 9) apoptosis pathways (Fig. 5). Cells were treated with an effective dose of BP-C1(750 µg/ml), lysed and subjected to western blot analysis for cleaved caspases 8 (Fig. 5A) and 9 (Fig. 5C) after 48 h of treatment, results indicate the appearance of the cleaved active subunit of caspase 8 (43 kDa) and caspase 9 (35 kDa), however the level of actin did not changed (Fig. 5. B and D).


Benzene-poly-carboxylic acid complex, a novel anti-cancer agent induces apoptosis in human breast cancer cells.

Fares F, Azzam N, Fares B, Larsen S, Lindkaer-Jensen S - PLoS ONE (2014)

Activation of caspase 8 (A) and caspase 9 (C) by BP-C1.Cells were treated with or without 750/ml of BP-C1 for 48 h. Cells were harvested and lysed. Activation of caspase-9 was determined by Western blotting as described under “Materials of Methods”. TA represents paclitaxel and 32c refers to Lx2-32c. Columns represent the densitometry analysis of the indicated proteins. The level of actin in the cells is represented in B and D.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3921106&req=5

pone-0085156-g005: Activation of caspase 8 (A) and caspase 9 (C) by BP-C1.Cells were treated with or without 750/ml of BP-C1 for 48 h. Cells were harvested and lysed. Activation of caspase-9 was determined by Western blotting as described under “Materials of Methods”. TA represents paclitaxel and 32c refers to Lx2-32c. Columns represent the densitometry analysis of the indicated proteins. The level of actin in the cells is represented in B and D.
Mentions: To further investigate the mechanistic action of cell death induced by BP-C1, a western blot analysis was performed to detect proteins that have been shown to be involved in both the extrinsic (caspase 8) and intrinsic (caspase 9) apoptosis pathways (Fig. 5). Cells were treated with an effective dose of BP-C1(750 µg/ml), lysed and subjected to western blot analysis for cleaved caspases 8 (Fig. 5A) and 9 (Fig. 5C) after 48 h of treatment, results indicate the appearance of the cleaved active subunit of caspase 8 (43 kDa) and caspase 9 (35 kDa), however the level of actin did not changed (Fig. 5. B and D).

Bottom Line: Caspases were detected by western blot analysis and gene expression was measured by using the Applied Biosystems® TaqMan® Array Plates.The results showed that exposure of the cells to BP-C1 for 48 h, significantly (P<0.001) reduced cell viability, induced apoptosis and activated caspase 8 and caspace 9.Moreover, gene expression experiments indicated that BP-C1 increased the expression of pro-apoptotic genes (CASP8AP1, TNFRSF21, NFkB2, FADD, BCL10 and CASP8) and lowered the level of mRNA transcripts of inhibitory apoptotic genes (BCL2L11, BCL2L2 and XIAP.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Biology, Faculty of Natural Sciences, University of Haifa, and Department of Molecular Genetics, Carmel Medical Center, Haifa, Israel.

ABSTRACT
Some cases of breast cancer are composed of clones of hormonal-independent growing cells, which do not respond to therapy. In the present study, the effect of Benzene-Poly-Carboxylic Acid Complex (BP-C1) on growth of human breast-cancer cells was tested. BP-C1 is a novel anti-cancer complex of benzene-poly-carboxylic acids with a very low concentration of cis-diammineplatinum (II) dichloride. Human breast cancer cells, MCF-7 and T47D, were used. Cell viability was detected by XTT assay and apoptosis was detected by Flow Cytometry and by annexin V/FITC/PI assay. Caspases were detected by western blot analysis and gene expression was measured by using the Applied Biosystems® TaqMan® Array Plates. The results showed that exposure of the cells to BP-C1 for 48 h, significantly (P<0.001) reduced cell viability, induced apoptosis and activated caspase 8 and caspace 9. Moreover, gene expression experiments indicated that BP-C1 increased the expression of pro-apoptotic genes (CASP8AP1, TNFRSF21, NFkB2, FADD, BCL10 and CASP8) and lowered the level of mRNA transcripts of inhibitory apoptotic genes (BCL2L11, BCL2L2 and XIAP. These findings may lead to the development of new therapeutic strategies for treatment of human cancer using BP-C1 analog.

Show MeSH
Related in: MedlinePlus