Effects of Atorvastatin on Proliferation and Expression of COX-2 Protein in Hepatic Cancer Cells
Yuheng Zhang
Abstract
Yuheng Zhang
Abstract
Objective: To investigate the effect of atorvastatin on the proliferation, cell cycle and COX -2 protein expression of human hepatocellular carcinoma (HepG2) cells in vitro. Methods: The human hepatocellular carcinoma HepG2 cells were employed during logarithmic growth phase and atorvastatin were added at the final concentrations of 0, 0.1, 1, 10 and 100 μmol/L respectively. The proliferation of the cells was detected by cell counting and MTT assay. The cell cycle was measured by flowcytometry (FCM). The COX -2 protein expression was detected by immunocytochemistry. Results: Atorvastatin suppressed the growth of HepG2 cells in a concentration - and time -dependent manner, but there was no significant difference between 0.1 μmol/L group and 0 μmol/L group. The cell cycle analysis revealed that atorvastatin caused a concentration-dependent increase of cells in G0/G1 phase cell cycle. At the same time the cells in S and G2/M phase were decreased. However, apoptosis was not obvious in HepG2 cells. Atorvastatin inhibited COX -2 protein expression in a concentration-dependent manner. Conclusion: Atorvastatin inhibited HepG2 cell growth in vitro, which may be related to its inhibitory effect on COX-2 protein expression and arresting HepG2 cells at G0/G1 phase cell cycle.
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Objective: To investigate the effect of atorvastatin on the proliferation, cell cycle and COX -2 protein expression of human hepatocellular carcinoma (HepG2) cells in vitro. Methods: The human hepatocellular carcinoma HepG2 cells were employed during logarithmic growth phase and atorvastatin were added at the final concentrations of 0, 0.1, 1, 10 and 100 μmol/L respectively. The proliferation of the cells was detected by cell counting and MTT assay. The cell cycle was measured by flowcytometry (FCM). The COX -2 protein expression was detected by immunocytochemistry. Results: Atorvastatin suppressed the growth of HepG2 cells in a concentration - and time -dependent manner, but there was no significant difference between 0.1 μmol/L group and 0 μmol/L group. The cell cycle analysis revealed that atorvastatin caused a concentration-dependent increase of cells in G0/G1 phase cell cycle. At the same time the cells in S and G2/M phase were decreased. However, apoptosis was not obvious in HepG2 cells. Atorvastatin inhibited COX -2 protein expression in a concentration-dependent manner. Conclusion: Atorvastatin inhibited HepG2 cell growth in vitro, which may be related to its inhibitory effect on COX-2 protein expression and arresting HepG2 cells at G0/G1 phase cell cycle.
Key concepts: Atorvastatin, Cell cycle, Cell growth, Apoptosis, Cancer cell, Cell, Chemistry, Immunocytochemistry