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毛蕊异黄酮通过 BATF/TGF-β1 抑制 EMT 抑制乳腺癌细胞迁移和侵袭。

Calycosin inhibits breast cancer cell migration and invasion by suppressing EMT via BATF/TGF-β1.

机构信息

School of Life Sciences and Food Engineering, Hanshan Normal University, Chaozhou 521041, Guangdong, China.

Center of Reproductive Medicine, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi, China.

出版信息

Aging (Albany NY). 2021 Jun 7;13(12):16009-16023. doi: 10.18632/aging.203093.

DOI:10.18632/aging.203093
PMID:34096887
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8266341/
Abstract

In this study, we investigated the effects of calycosin on breast cancer cell progression and their underlying mechanisms. Calycosin dose- and time-dependently inhibited proliferation, migration, and invasion by T47D and MCF-7 breast cancer cells by downregulating basic leucine zipper ATF-like transcription factor (BATF) expression. Moreover, BATF promoted breast cancer cell migration and invasiveness by increasing TGFβ1 mRNA and protein levels. Bioinformatics analysis, dual luciferase reporter assays, and chromatin immunoprecipitation assays confirmed the presence of BATF-binding sites in the promoter sequence of gene. Calycosin treatment inhibited epithelial-mesenchymal transition (EMT) of breast cancer cells by significantly increasing E-cadherin levels and decreasing N-cadherin, Vimentin, CD147, MMP-2, and MMP-9 levels through downregulation of BATF and TGFβ1. TGFβ1 knockdown reduced the migration and invasiveness of BATF-overexpressing breast cancer cells, whereas incubation with TGFβ1 enhanced the migration and invasiveness of calycosin-treated breast cancer cells. Our findings demonstrated that calycosin inhibited EMT and progression of breast cancer cells by suppressing BATF/TGFβ1 signaling. This suggests calycosin would be a promising therapeutic option for breast cancer patients.

摘要

在这项研究中，我们研究了毛蕊异黄酮对乳腺癌细胞进展的影响及其潜在机制。毛蕊异黄酮通过下调碱性亮氨酸拉链 ATF 样转录因子（BATF）的表达，呈剂量和时间依赖性地抑制 T47D 和 MCF-7 乳腺癌细胞的增殖、迁移和侵袭。此外，BATF 通过增加 TGFβ1 mRNA 和蛋白水平促进乳腺癌细胞的迁移和侵袭。生物信息学分析、双荧光素酶报告基因检测和染色质免疫沉淀实验证实了 基因启动子序列中存在 BATF 结合位点。毛蕊异黄酮通过下调 BATF 和 TGFβ1，显著增加 E-钙黏蛋白水平，降低 N-钙黏蛋白、波形蛋白、CD147、MMP-2 和 MMP-9 水平，抑制乳腺癌细胞的上皮-间充质转化（EMT）。TGFβ1 敲低降低了 BATF 过表达的乳腺癌细胞的迁移和侵袭能力，而 TGFβ1 的孵育增强了毛蕊异黄酮处理的乳腺癌细胞的迁移和侵袭能力。我们的研究结果表明，毛蕊异黄酮通过抑制 BATF/TGFβ1 信号通路抑制 EMT 和乳腺癌细胞的进展。这表明毛蕊异黄酮可能成为乳腺癌患者有前途的治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56d7/8266341/916c383cc753/aging-13-203093-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56d7/8266341/da4cbea73d53/aging-13-203093-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56d7/8266341/916c383cc753/aging-13-203093-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56d7/8266341/da4cbea73d53/aging-13-203093-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56d7/8266341/db7747ccfc7c/aging-13-203093-g002.jpg
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