Antiproliferative Activity of Ursolic Acid in MDA-MB-231 Human Breast Cancer Cells through Nrf2 Pathway Regulation.,Journal of Agricultural and Food Chemistry

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Antiproliferative Activity of Ursolic Acid in MDA-MB-231 Human Breast Cancer Cells through Nrf2 Pathway Regulation.
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2020-06-18 , DOI: 10.1021/acs.jafc.0c03202
Xi Zhang ₁ , Tong Li ₁ , Er Sheng Gong _{1,

2} , Rui Hai Liu _{1,

3}

Affiliation

The potential mechanisms of action of ursolic acid (UA) in regulating cell proliferation in MDA-MB-231 human breast cancer cells through Nrf2 pathway were investigated. UA significantly inhibited the proliferation of MDA-MB-231 cells at a dose ≥10 μM in a dose-dependent manner, and no cytotoxicity was observed at concentrations below 29.87 ± 2.60 μM. The expressions of Nrf2 and p-Nrf2, in whole cell and nucleus, and NQO1 were inhibited by UA treatment, whereas the Keap1 expression was upregulated. No significant difference was observed in the Nrf2 mRNA levels, indicating that UA reduced Nrf2 expression not through mRNA but through a post-translational mechanism. Additionally, EGF-induced p-Nrf2 and its downstream NQO1 and SOD1 enzymes were abolished by UA. However, EGF or p-EGFR had no effect on the expressions of Keap1. These results suggested that the proliferative inhibitory effect of UA might be partially through downregulating Nrf2 via the Keap1/Nrf2 pathway and EGFR/Nrf2 pathway in MDA-MB-231 cells.

中文翻译：

熊果酸通过 Nrf2 途径调节 MDA-MB-231 人乳腺癌细胞的抗增殖活性。

研究了熊果酸（UA）通过 Nrf2 途径调节 MDA-MB-231 人乳腺癌细胞增殖的潜在作用机制。 UA在剂量≥10 μM时显着抑制MDA-MB-231细胞的增殖，且呈剂量依赖性，在浓度低于29.87 ± 2.60 μM时未观察到细胞毒性。 UA处理抑制全细胞和细胞核中Nrf2和p -Nrf2以及NQO1的表达，而Keap1表达上调。 Nrf2 mRNA 水平没有观察到显着差异，表明 UA 不是通过 mRNA 而是通过翻译后机制降低 Nrf2 表达。此外，UA 还消除了 EGF 诱导的p -Nrf2 及其下游 NQO1 和 SOD1 酶。然而，EGF或p -EGFR对Keap1的表达没有影响。这些结果表明，UA的增殖抑制作用可能部分是通过Keap1/Nrf2通路和EGFR/Nrf2通路下调MDA-MB-231细胞中的Nrf2而实现的。

更新日期：2020-07-15

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