Oxaloacetate induces apoptosis in HepG2 cells via inhibition of glycolysis

被引：28

作者：

Kuang, Ye ^{[1
]}

Han, Xiaoyun ^{[1
]}

Xu, Mu ^{[1
]}

Yang, Qing ^{[1
]}

机构：

[1] Jilin Univ, Coll Basic Med Sci, Dept Pathogenobiol, 126 Xinmin St, Changchun 130021, Jilin, Peoples R China

来源：

CANCER MEDICINE | 2018年 / 7卷 / 04期

基金：

中国国家自然科学基金;

关键词：

Akt; HIF pathway; apoptosis; glycolysis; oxaloacetate; oxidative phosphorylation; CANCER-CELLS; METABOLIC PATHWAYS; HYPOXIA; PROLIFERATION; HYDROXYLASES; ACIDOSIS; SWITCH; HIF-1;

D O I：

10.1002/cam4.1410

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Most cancer cells perform glycolysis despite having sufficient oxygen. The specific metabolic pathways of cancer cells have become the focus of cancer treatment. Recently, accumulating evidence indicates oxidative phosphorylation (OXPHOS) and glycolysis can be regulated with each other. Thus, we suggest that the glycolysis of cancer cells is inhibited by restoring or improving OXPHOS in cancer cells. In our study, we found that oxaloacetate (OA) induced apoptosis in HepG2 cells in vivo and in vitro. Meanwhile, we found that OA induced a decrease in the energy metabolism of HepG2 cells. Further results showed that the expression and activity of glycolytic enzymes were decreased with OA treatment. Conversely, the expression and activity of enzymes involved in the TCA cycle and OXPHOS were increased with OA treatment. The results indicate that OA can inhibit glycolysis through enhancement of OXPHOS. In addition, OA-mediated suppression of HIF1, p-Akt, and c-myc led to a decrease in glycolysis level. Therefore, OA has the potential to be a novel anticancer drug.

引用

页码：1416 / 1429

页数：14

共 52 条

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