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通过膜联蛋白A1促进转化生长因子-β诱导的三阴性乳腺癌细胞上皮-间质转化并增强其化疗耐药性。

Promotes TGF-β-Induced Epithelial-Mesenchymal Transition and Enhances Chemoresistance in Triple-Negative Breast Cancer Cells via ANXA1.

作者信息

Tang Li, Chen Yuli, Chen Huanhuan, Jiang Pan, Yan Linping, Mo Dongping, Tang Xun, Yan Feng

机构信息

Department of Clinical Laboratory, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & the Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, China.

Department of Clinical Laboratory, Nanjing Qixia District Hospital, Nanjing, China.

出版信息

Front Oncol. 2020 Mar 12;10:280. doi: 10.3389/fonc.2020.00280. eCollection 2020.

DOI:10.3389/fonc.2020.00280
PMID:32226772
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7080863/
Abstract

Triple-negative breast cancer (TNBC) is a highly metastatic breast cancer subtype, and the primary systemic treatment strategy involves conventional chemotherapy. DC-STAMP domain containing 1-antisense 1 () is a long non-coding RNA that promotes TNBC migration and invasion. Studying the role of in promoting epithelial-mesenchymal transition (EMT) and chemoresistance will provide a new strategy for TNBC therapy. In the present study, we found that regulates the expression or secretion of EMT-related proteins E-cadherin, snail family zinc finger 1 (SNAI1), vimentin, matrix metallopeptidase 2 (MMP2), and matrix metallopeptidase 9 (MMP9). Interference with impaired TGF-β-induced TNBC cell invasion and migration. directly binds to ANXA1 in BT-549 cells and affects the expression of ANXA1. enhances TGF-β/Smad signaling in BT-549 cells through ANXA1 to promote EMT. The combination of and ANXA1 also contributes to enhancement of the resistance of BT-549 cells to doxorubicin and paclitaxel. In conclusion, promotes TGF-β-induced EMT and enhances chemoresistance in TNBC cells through ANXA1, and therefore represents a potentially promising target for metastatic breast cancer therapy.

摘要

三阴性乳腺癌（TNBC）是一种具有高度转移性的乳腺癌亚型，主要的全身治疗策略包括传统化疗。含DC-STAMP结构域1反义1（）是一种长链非编码RNA，可促进TNBC的迁移和侵袭。研究其在促进上皮-间质转化（EMT）和化疗耐药中的作用将为TNBC治疗提供新策略。在本研究中，我们发现其调节EMT相关蛋白E-钙黏蛋白、蜗牛家族锌指蛋白1（SNAI1）、波形蛋白、基质金属蛋白酶2（MMP2）和基质金属蛋白酶9（MMP9）的表达或分泌。干扰其会损害转化生长因子-β（TGF-β）诱导的TNBC细胞侵袭和迁移。其在BT-549细胞中直接与膜联蛋白A1（ANXA1）结合并影响ANXA1的表达。其通过ANXA1增强BT-549细胞中的TGF-β/Smad信号传导以促进EMT。其与ANXA1的联合也有助于增强BT-549细胞对阿霉素和紫杉醇的耐药性。总之，其通过ANXA1促进TGF-β诱导的EMT并增强TNBC细胞的化疗耐药性，因此是转移性乳腺癌治疗的一个潜在有前景的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9157/7080863/cf2af4e243bf/fonc-10-00280-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9157/7080863/73bb471c36f4/fonc-10-00280-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9157/7080863/cf2af4e243bf/fonc-10-00280-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9157/7080863/73bb471c36f4/fonc-10-00280-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9157/7080863/8ef8dd2bad38/fonc-10-00280-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9157/7080863/8f1e5acea831/fonc-10-00280-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9157/7080863/a6c44c5a07e5/fonc-10-00280-g0004.jpg
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