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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 the proliferation of human hepatocarcinoma HepG-2 cells. Figure 3 shows the effect of different doses of β-ELE on cell proliferation at different time periods. β-ELE significantly decreased the growth of HepG-2 cells compared with the control group. The IC50s were 96.13, 80.84, and 60.95 μg/mL for 24, 48, and 72 h, respectively, and the inhibitory effect was dose- and time-dependent.
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fig3: The effects of β-ELE (β-Elemene) on the proliferation of human hepatocarcinoma HepG-2 cells. Figure 3 shows the effect of different doses of β-ELE on cell proliferation at different time periods. β-ELE significantly decreased the growth of HepG-2 cells compared with the control group. The IC50s were 96.13, 80.84, and 60.95 μg/mL for 24, 48, and 72 h, respectively, and the inhibitory effect was dose- and time-dependent.

Mentions: As shown in Figure 3, the cell proliferation rate was affected by increasing β-ELE concentrations at different time intervals. β-ELE significantly decreased the growth of HepG-2 cells compared with the control group. The IC50s were 96.13, 80.84, and 60.95 μg/mL for 24, 48, and 72 h, respectively, and the inhibitory effect was dose- and time-dependent. These data indicate that β-ELE has an inhibitory effect on the proliferation of HepG-2 cells.


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 the proliferation of human hepatocarcinoma HepG-2 cells. Figure 3 shows the effect of different doses of β-ELE on cell proliferation at different time periods. β-ELE significantly decreased the growth of HepG-2 cells compared with the control group. The IC50s were 96.13, 80.84, and 60.95 μg/mL for 24, 48, and 72 h, respectively, and the inhibitory effect was dose- and time-dependent.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4499621&req=5

fig3: The effects of β-ELE (β-Elemene) on the proliferation of human hepatocarcinoma HepG-2 cells. Figure 3 shows the effect of different doses of β-ELE on cell proliferation at different time periods. β-ELE significantly decreased the growth of HepG-2 cells compared with the control group. The IC50s were 96.13, 80.84, and 60.95 μg/mL for 24, 48, and 72 h, respectively, and the inhibitory effect was dose- and time-dependent.
Mentions: As shown in Figure 3, the cell proliferation rate was affected by increasing β-ELE concentrations at different time intervals. β-ELE significantly decreased the growth of HepG-2 cells compared with the control group. The IC50s were 96.13, 80.84, and 60.95 μg/mL for 24, 48, and 72 h, respectively, and the inhibitory effect was dose- and time-dependent. These data indicate that β-ELE has an inhibitory effect on the proliferation of HepG-2 cells.

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