Apatinib Suppresses Proliferation and Induced Apoptosis of Human Breast Cancer Cell Line MDA-MB-231 Through Glycolytic Inhibition
Objective To investigate the antitumor effect of apatinib on breast cancer cells in vitro and its mechanism. Methods CCK-8 assay was used to detect the inhibitory effect of apatinib on the proliferation of breast cancer cell line MDA-MB-231. Annexin V-FITC/PI apoptosis detection kit was used to dete...
Main Authors: | , , , |
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Format: | Article |
Language: | zho |
Published: |
Magazine House of Cancer Research on Prevention and Treatment
2019-05-01
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Series: | Zhongliu Fangzhi Yanjiu |
Subjects: | |
Online Access: | http://html.rhhz.net/ZLFZYJ/html/8578.2019.18.1422.htm |
Summary: | Objective To investigate the antitumor effect of apatinib on breast cancer cells in vitro and its mechanism. Methods CCK-8 assay was used to detect the inhibitory effect of apatinib on the proliferation of breast cancer cell line MDA-MB-231. Annexin V-FITC/PI apoptosis detection kit was used to detect the effect of apatinib on the apoptosis of MDA-MB-231 cells. The effect of apatinib on lactate production in MDA-MB-231 cells was detected by lactate content assay kit. The effect of apatinib on the extracellular acidification rate of MDA-MB-231 cells was detected by glycolysis stress test kit. Results Apatinib inhibited the proliferation of breast cancer MDA-MB-231 cells in vitro in a concentration-dependent manner (P < 0.05). The half maximal inhibitory concentration (IC50) of apatinib in MDA-MB-231 cells was 1.56μmol/L for 48h treatment. Apatinib also induced the apoptosis of MDA-MB-231 cells in a concentration-dependent manner (P < 0.05). Apatinib inhibited intracellular lactate content in MDA-MB-231 cells in a concentration-dependent manner (P < 0.05). Apatinib also decreased extracellular acidification rate of MDA-MB-231 cells, including glycolytic capacity and glycolytic reserve (P < 0.05). Conclusion Apatinib could induce the apoptosis of breast cancer cell line MDA-MB-231 by inhibiting aerobic glycolysis. |
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ISSN: | 1000-8578 1000-8578 |