Toosendanin Inhibits Glycolysis in Breast Cancer by Regulating Pyruvate Kinase M

WANG Hong-lei; XIAO Yi; WU Li; MA Da-chang

doi:10.13422/j.cnki.syfjx.20180796

您当前的位置：

首页 >

文章列表页 >

Toosendanin Inhibits Glycolysis in Breast Cancer by Regulating Pyruvate Kinase M

更新时间：2024-01-04

- Toosendanin Inhibits Glycolysis in Breast Cancer by Regulating Pyruvate Kinase M
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 24, Issue 7, Pages: 177-183(2018)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20180796
  CLC： R285
- Published：2018
- 稿件说明：
移动端阅览
WANG Hong-lei, XIAO Yi, WU Li, et al. Toosendanin Inhibits Glycolysis in Breast Cancer by Regulating Pyruvate Kinase M[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(7): 177-183.
DOI：

WANG Hong-lei, XIAO Yi, WU Li, et al. Toosendanin Inhibits Glycolysis in Breast Cancer by Regulating Pyruvate Kinase M[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(7): 177-183. DOI： 10.13422/j.cnki.syfjx.20180796.

摘要

目的：观察川楝素对乳腺癌糖酵解的干预及糖酵解相关酶的影响。方法：采用人乳腺癌细胞株MDA-MB-231，MCF-7；通过噻唑蓝（MTT）比色法考察川楝素（0，2.5，5，10，20，40，60，80 μmol ·L-1）对乳腺癌细胞增殖的抑制作用，检测10，20，40 μmol ·L-1川楝素干预后乳腺癌细胞中葡萄糖消耗，乳酸含量，评价川楝素对乳腺癌细胞糖酵解的干预作用；检测乳腺癌细胞中三磷酸腺苷（ATP）及烟酰胺腺嘌呤二核苷酸（NAD+）/还原型烟酰胺腺嘌呤二核苷酸磷酸（NADH）水平，评价乳腺癌细胞能量供应水平；检测己糖激酶2及丙酮酸激酶活性，考察川楝素对糖酵解相关酶活性影响。蛋白免疫印迹法检测川楝素对乳腺癌细胞中丙酮酸激酶M2蛋白表达的调控作用。结果：川楝素对人乳腺癌MDA-MB-231，MCF-7细胞增殖具有明显抑制作用（P<0.05），并呈浓度依赖性；川楝素可以明显降低不同乳腺癌细胞株中葡萄糖消耗及乳酸含量（P<0.05），并降低细胞ATP含量（P<0.05），升高NAD+/NADH含量（P<0.05），抑制肿瘤细胞糖酵解水平。此外川楝素可抑制丙酮酸激酶活性，但对己糖激酶2活性无影响，蛋白检测结果表明，川楝素可以下调丙酮酸激酶M2蛋白表达水平（P<0.05）。结论：川楝素可以明显抑制乳腺癌细胞增殖，并影响乳腺癌细胞糖酵解水平，其机制与其干预乳腺癌细胞中丙酮酸激酶M2的表达相关。

Abstract

Objective: To investigate the effects of toosendanin on the glycolysis of breast cancer cells and the effect on glycolytic enzymes. Method: The human breast cancer cell line MDA-MB-231

MCF-7 were used in this experiment; the inhibitory effect of different concentrations of toosendanin (0

2.5

80 μmol · L-1) on MDA-MB-231and MCF-7 cells proliferation was investigated by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay. Glucose consumption and lactate content in MDA-MB-231 and MCF-7 cells were also detected after treatment with 10

40 μmol · L-1 toosendanin to evaluate its intervention effect on glycolysis of breast cancer cells. The levels of adenosine triphosphate (ATP) and nicotinamide adenine dinucleotide (NAD+)/reduced nicotinamide adenine dinucleotide phosphate (NADH) in breast cancer cells were detected to evaluate the cell energy supply level. Hexokinase and pyruvate kinase activities were detected to evaluate the effect of toosendanin on glycolytic enzyme activity. Western blot was used to detect the regulatory effect of toosendanin on pyruvate kinase M2 protein expression in breast cancer cells. Result: The results showed that toosendanin had obvious inhibitory effect on cell proliferation in MDA-MB-231and MCF-7 cells in a concentration dependent manner(P<0.05). Toosendanin could significantly reduce the consumption of glucose and lactic acid content in different breast cancer cell lines(P<0.05)

and reduce ATP content in cells(P<0.05)

increase the content of NAD+/NADH

and inhibit tumor cell glycolysis level (P<0.05). In addition

it could inhibit the activity of pyruvate kinase

but had no effect on the activity of hexokinase 2

and the results of quantitative analysis showed that the expression of pyruvate kinase M2 could be decreased(P<0.05). Conclusion: Toosendanin could significantly inhibit the proliferation of breast cancer cells and affect the level of glycolysis. Its mechanism may be associated with regulating the expression of pyruvate kinase M2 in breast cancer cells.

关键词

Keywords

references

Views

下载量

CSCD

Alert me when the article has been cited

提交

Tools

Publicity Resources

Danzhi Xiaoyaosan-containing Serum Reverses Energy Metabolic Reprogramming of MDA-MB-231 Breast Cancer Cells

Effect of Alternol on Glycolysisin in Mice Melanoma B16F0 Cells

Shaoyaotang Regulates Glucose Metabolism Reprogramming to Inhibit Macrophage Polarization Toward M1 Phenotype

Alleviation of Ulcerative Colitis by Shaoyaotang via Inhibiting Glycolysis Through SIRT6/HIF-1α Pathway

Molecular Mechanism of Treating Different Diseases with Same Treatment of Gypenoside L Affecting Oxidative Damage HUVEC and OVCAR-3 Through EGFR/STAT3/Glycolytic Pathway

Related Author

Shuang XU

Ran LI

Li-ping LIU

WANG Peng-long

MA Xiao-yi

ZHENG Qiu-sheng

JIANG Shaijin

CAO Hui

Related Institution

College of Traditional Chinese Medicine（TCM）， Liaoning University of TCM

The First Hospital of Hunan University of Chinese Medicine

Liaoning University of Traditional Chinese Medicine

Liaoning Cancer Hospital

Liaoning University of Traditional Chinese Medicine（TCM）

AI问答

Postal code：100700
Tel：010-84076882 Email：syfjx_2010@188.com
Technical support is provided by Beijing Founder electronics co., LTD 京ICP备11006657号-10 京公网安备11010802024621
It is recommended to read the content of this site in Chrome&IE9+. Please switch to extreme mode in browser 360.
Cookies We use cookies to help provide and enhance our service and tailor content. By continuing, you agree to the use of cookies.

⁰