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β-Elemene Inhibits Cell Proliferation by Regulating the Expression and Activity of Topoisomerases I and IIα in Human Hepatocarcinoma HepG-2 Cells.

Gong M, Liu Y, Zhang J, Gao YJ, Zhai PP, Su X, Li X, Li Y, Hou L, Cui XN - Biomed Res Int (2015)

Bottom Line: To investigate the effects of β-Elemene (β-ELE) on the proliferation, apoptosis, and topoisomerase I (TOPO I) and topoisomerase IIα (TOPO IIα) expression and activity of human hepatocarcinoma HepG-2 cells.After treatment with β-ELE, morphological alterations of HepG-2 cells were observed under an inverted microscope.Supercoiled pBR322 and kDNA were also used to determine the direct effect of β-ELE on DNA breaks. β-ELE significantly inhibited HepG-2 cell proliferation in a dose- and time-dependent manner. β-ELE also induced tumor cell arrest at S phase, induced cell apoptosis, and downregulated the protein expression of TOPO I and TOPO IIα in a dose-dependent manner. β-ELE also inhibited TOPO I- and TOPO IIα-mediated DNA relaxation but did not directly induce DNA breakage at any concentration. β-ELE could inhibit the proliferation of HepG-2 cells and interfere with the expression and activity of TOPO I and TOPO IIα.

View Article: PubMed Central - PubMed

Affiliation: Department of Oncology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, China.

ABSTRACT

Objective: To investigate the effects of β-Elemene (β-ELE) on the proliferation, apoptosis, and topoisomerase I (TOPO I) and topoisomerase IIα (TOPO IIα) expression and activity of human hepatocarcinoma HepG-2 cells.

Methods: After treatment with β-ELE, morphological alterations of HepG-2 cells were observed under an inverted microscope. Cell proliferation was assessed using an MTT assay, cell cycles were analyzed using flow cytometry, and apoptosis was detected by Annexin V/PI staining. The expression of TOPO I and TOPO IIα was analyzed by Western blot techniques, and their activity was measured using the TOPO I-mediated, supercoiled pBR322 DNA relaxation and TOPO IIα-mediated Kinetoplast DNA (kDNA) decatenation assays, respectively. Supercoiled pBR322 and kDNA were also used to determine the direct effect of β-ELE on DNA breaks.

Results: β-ELE significantly inhibited HepG-2 cell proliferation in a dose- and time-dependent manner. β-ELE also induced tumor cell arrest at S phase, induced cell apoptosis, and downregulated the protein expression of TOPO I and TOPO IIα in a dose-dependent manner. β-ELE also inhibited TOPO I- and TOPO IIα-mediated DNA relaxation but did not directly induce DNA breakage at any concentration.

Conclusion: β-ELE could inhibit the proliferation of HepG-2 cells and interfere with the expression and activity of TOPO I and TOPO IIα.

No MeSH data available.


Related in: MedlinePlus

The effects of β-ELE (β-Elemene) on TOPO I and TOPO IIα protein expression in HepG-2 cells. (a) Western blot analysis showed that both the ratios of TOPO I/β-actin (0.960 ± 0.036, 0.759 ± 0.034, and 0.591 ± 0.049) and TOPO IIα/β-actin (0.937 ± 0.029, 0.752 ± 0.015, and 0.600 ± 0.017) were significantly decreased in a dose-dependent manner after β-ELE treatment (0, 20, 40, and 60 μg/mL, P < 0.05). (b) The ratios of TOPO I/β-actin (0.960 ± 0.036, 0.759 ± 0.034, and 0.591 ± 0.049) were significantly lower than that of the control group (1.161 ± 0.043); and the ratios of TOPO IIα/β-actin (0.937 ± 0.029, 0.752 ± 0.015, and 0.600 ± 0.017) were significantly lower than that of the control group (1.134 ± 0.045) (∗∗P < 0.005, ∗∗∗P < 0.001). These results suggest that the expression of the TOPO I and TOPO IIα proteins significantly decreased in a dose-dependent manner after β-ELE treatment.
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fig5: The effects of β-ELE (β-Elemene) on TOPO I and TOPO IIα protein expression in HepG-2 cells. (a) Western blot analysis showed that both the ratios of TOPO I/β-actin (0.960 ± 0.036, 0.759 ± 0.034, and 0.591 ± 0.049) and TOPO IIα/β-actin (0.937 ± 0.029, 0.752 ± 0.015, and 0.600 ± 0.017) were significantly decreased in a dose-dependent manner after β-ELE treatment (0, 20, 40, and 60 μg/mL, P < 0.05). (b) The ratios of TOPO I/β-actin (0.960 ± 0.036, 0.759 ± 0.034, and 0.591 ± 0.049) were significantly lower than that of the control group (1.161 ± 0.043); and the ratios of TOPO IIα/β-actin (0.937 ± 0.029, 0.752 ± 0.015, and 0.600 ± 0.017) were significantly lower than that of the control group (1.134 ± 0.045) (∗∗P < 0.005, ∗∗∗P < 0.001). These results suggest that the expression of the TOPO I and TOPO IIα proteins significantly decreased in a dose-dependent manner after β-ELE treatment.

Mentions: After treatment with different doses of β-ELE for 48 h, a dose-dependent decrease in the protein expression of TOPO I and TOPO IIα in HepG-2 cells was observed, as shown in Figure 5. The ratio of TOPO I/β-actin (0.960 ± 0.036, 0.759 ± 0.034, and 0.591 ± 0.049, resp.) was significantly lower than that of the control group (1.161 ± 0.043) (P < 0.05), and the ratio of TOPO IIα/β-actin (0.937 ± 0.029, 0.752 ± 0.015, and 0.600 ± 0.017, resp.) was significantly lower than that of the control group (1.134 ± 0.045) (P < 0.05). These results suggest that the expression of TOPO I and TOPO IIα proteins significantly decreased in a dose-dependent manner after β-ELE treatment.


β-Elemene Inhibits Cell Proliferation by Regulating the Expression and Activity of Topoisomerases I and IIα in Human Hepatocarcinoma HepG-2 Cells.

Gong M, Liu Y, Zhang J, Gao YJ, Zhai PP, Su X, Li X, Li Y, Hou L, Cui XN - Biomed Res Int (2015)

The effects of β-ELE (β-Elemene) on TOPO I and TOPO IIα protein expression in HepG-2 cells. (a) Western blot analysis showed that both the ratios of TOPO I/β-actin (0.960 ± 0.036, 0.759 ± 0.034, and 0.591 ± 0.049) and TOPO IIα/β-actin (0.937 ± 0.029, 0.752 ± 0.015, and 0.600 ± 0.017) were significantly decreased in a dose-dependent manner after β-ELE treatment (0, 20, 40, and 60 μg/mL, P < 0.05). (b) The ratios of TOPO I/β-actin (0.960 ± 0.036, 0.759 ± 0.034, and 0.591 ± 0.049) were significantly lower than that of the control group (1.161 ± 0.043); and the ratios of TOPO IIα/β-actin (0.937 ± 0.029, 0.752 ± 0.015, and 0.600 ± 0.017) were significantly lower than that of the control group (1.134 ± 0.045) (∗∗P < 0.005, ∗∗∗P < 0.001). These results suggest that the expression of the TOPO I and TOPO IIα proteins significantly decreased in a dose-dependent manner after β-ELE treatment.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig5: The effects of β-ELE (β-Elemene) on TOPO I and TOPO IIα protein expression in HepG-2 cells. (a) Western blot analysis showed that both the ratios of TOPO I/β-actin (0.960 ± 0.036, 0.759 ± 0.034, and 0.591 ± 0.049) and TOPO IIα/β-actin (0.937 ± 0.029, 0.752 ± 0.015, and 0.600 ± 0.017) were significantly decreased in a dose-dependent manner after β-ELE treatment (0, 20, 40, and 60 μg/mL, P < 0.05). (b) The ratios of TOPO I/β-actin (0.960 ± 0.036, 0.759 ± 0.034, and 0.591 ± 0.049) were significantly lower than that of the control group (1.161 ± 0.043); and the ratios of TOPO IIα/β-actin (0.937 ± 0.029, 0.752 ± 0.015, and 0.600 ± 0.017) were significantly lower than that of the control group (1.134 ± 0.045) (∗∗P < 0.005, ∗∗∗P < 0.001). These results suggest that the expression of the TOPO I and TOPO IIα proteins significantly decreased in a dose-dependent manner after β-ELE treatment.
Mentions: After treatment with different doses of β-ELE for 48 h, a dose-dependent decrease in the protein expression of TOPO I and TOPO IIα in HepG-2 cells was observed, as shown in Figure 5. The ratio of TOPO I/β-actin (0.960 ± 0.036, 0.759 ± 0.034, and 0.591 ± 0.049, resp.) was significantly lower than that of the control group (1.161 ± 0.043) (P < 0.05), and the ratio of TOPO IIα/β-actin (0.937 ± 0.029, 0.752 ± 0.015, and 0.600 ± 0.017, resp.) was significantly lower than that of the control group (1.134 ± 0.045) (P < 0.05). These results suggest that the expression of TOPO I and TOPO IIα proteins significantly decreased in a dose-dependent manner after β-ELE treatment.

Bottom Line: To investigate the effects of β-Elemene (β-ELE) on the proliferation, apoptosis, and topoisomerase I (TOPO I) and topoisomerase IIα (TOPO IIα) expression and activity of human hepatocarcinoma HepG-2 cells.After treatment with β-ELE, morphological alterations of HepG-2 cells were observed under an inverted microscope.Supercoiled pBR322 and kDNA were also used to determine the direct effect of β-ELE on DNA breaks. β-ELE significantly inhibited HepG-2 cell proliferation in a dose- and time-dependent manner. β-ELE also induced tumor cell arrest at S phase, induced cell apoptosis, and downregulated the protein expression of TOPO I and TOPO IIα in a dose-dependent manner. β-ELE also inhibited TOPO I- and TOPO IIα-mediated DNA relaxation but did not directly induce DNA breakage at any concentration. β-ELE could inhibit the proliferation of HepG-2 cells and interfere with the expression and activity of TOPO I and TOPO IIα.

View Article: PubMed Central - PubMed

Affiliation: Department of Oncology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, China.

ABSTRACT

Objective: To investigate the effects of β-Elemene (β-ELE) on the proliferation, apoptosis, and topoisomerase I (TOPO I) and topoisomerase IIα (TOPO IIα) expression and activity of human hepatocarcinoma HepG-2 cells.

Methods: After treatment with β-ELE, morphological alterations of HepG-2 cells were observed under an inverted microscope. Cell proliferation was assessed using an MTT assay, cell cycles were analyzed using flow cytometry, and apoptosis was detected by Annexin V/PI staining. The expression of TOPO I and TOPO IIα was analyzed by Western blot techniques, and their activity was measured using the TOPO I-mediated, supercoiled pBR322 DNA relaxation and TOPO IIα-mediated Kinetoplast DNA (kDNA) decatenation assays, respectively. Supercoiled pBR322 and kDNA were also used to determine the direct effect of β-ELE on DNA breaks.

Results: β-ELE significantly inhibited HepG-2 cell proliferation in a dose- and time-dependent manner. β-ELE also induced tumor cell arrest at S phase, induced cell apoptosis, and downregulated the protein expression of TOPO I and TOPO IIα in a dose-dependent manner. β-ELE also inhibited TOPO I- and TOPO IIα-mediated DNA relaxation but did not directly induce DNA breakage at any concentration.

Conclusion: β-ELE could inhibit the proliferation of HepG-2 cells and interfere with the expression and activity of TOPO I and TOPO IIα.

No MeSH data available.


Related in: MedlinePlus