鸦胆子苦素D通过PI3K/Akt信号通路抑制人乳腺癌MDA-MB-231细胞的能量代谢研究

王雨; 罗璨; 吉兆宁

doi:10.13898/j.cnki.issn.1000-2200.2020.05.001

鸦胆子苦素D通过PI3K/Akt信号通路抑制人乳腺癌MDA-MB-231细胞的能量代谢研究

Bruceine D inhibits energy metabolism in human breast cancer MDA-MB-231 cells via the PI3K/Akt signaling pathway

摘要

摘要:
目的研究鸦胆子苦素D对乳腺癌MDA-MB-231细胞能量代谢的影响及作用机制。
方法通过MTT法检测鸦胆子苦素D对细胞活力的影响。通过试剂盒测定葡萄糖消耗量、乳酸生成量、ATP含量和己糖激酶(HK)、磷酸果糖激酶(PFK)、丙酮酸激酶(PK)、乳酸脱氢酶(LDH)活性。Western blotting检测鸦胆子苦素D对PI3K、Akt、p-Akt蛋白表达水平的影响。

结果鸦胆子苦素D可浓度依赖性地抑制MDA-MB-231细胞的增殖活性(P＜0.01)。与对照组相比，1、2、4 μmol/L鸦胆子苦素D均可降低MDA-MB-231细胞中ATP含量, 减少葡萄糖消耗量和乳酸生成量, 降低HK、PFK、PK和LDH的活性(P＜0.05)；2、4 μmol/L鸦胆子苦素D可抑制细胞中PI3K、p-Akt蛋白的表达(P＜0.05)。

结论鸦胆子苦素D抑制人乳腺癌MDA-MB-231细胞PI3K/Akt信号通路，进而抑制有氧糖酵解过程，减少细胞能量供应。

Abstract:
Objective To investigate the effect of bruceine D on energy metabolism in breast cancer MDA-MB-231 cells and its mechanism.

Methods MTT assay was used to detect the effect of bruceine D on cell viability.Glucose consumption, lactate production, ATP content and activities of hexokinase (HK), phosphofructokinase (PFK), pyruvate kinase (PK) and lactate dehydrogenase (LDH) were determined by kits.Western blotting was used to analyze the effect of bruceine D on the expression of PI3K, Akt and p-Akt protein.

Results Bruceine D inhibited the proliferation of MDA-MB-231 cells at a concentration-dependent manner (P<0.01).Compared with the control group, bruceine D (1, 2, 4 μmol/L) could reduce the ATP content, glucose consumption, lactate production, and the activities of HK, PFK, PK and LDH in MDA-MB-231 cells (P<0.05);2, 4 μmol/L bruceine D could inhibit the expression of PI3K and p-Akt protein in MDA-MB-231 cells (P<0.05).

Conclusions Bruceine D inhibits the PI3K/Akt signaling pathway in human breast cancer MDA-MB-231 cells, then suppresses the aerobic glycolysis and reduces cells' energy supply.

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