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Wnt 共受体低密度脂蛋白受体相关蛋白 6（LRP6）在三阴性乳腺癌细胞迁移和侵袭中的作用

Role of Wnt Co-Receptor LRP6 in Triple Negative Breast Cancer Cell Migration and Invasion.

作者信息

Ma Jinlu, Lu Wenyan, Chen Dongquan, Xu Bo, Li Yonghe

机构信息

Department of Radiation Oncology, the First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, 710061, Shaanxi, China.

Drug Discovery Division, Department of Oncology, Southern Research Institute, Birmingham, Alabama, 35255.

出版信息

J Cell Biochem. 2017 Sep;118(9):2968-2976. doi: 10.1002/jcb.25956. Epub 2017 May 30.

DOI:10.1002/jcb.25956
PMID:28247948
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10928515/
Abstract

The low-density lipoprotein receptor-related protein 6 (LRP6) is an essential Wnt co-receptor of the Wnt/β-catenin signaling pathway. Although studies have shown an increased expression of LRP6 in several types of cancer, its function in tumor development and progression remains to be elucidated. We herein demonstrated that LRP6 expression is up-regulated in human triple negative breast cancer (TNBC) patients and human TNBC cell lines, and that knockdown of LRP6 expression and treatment of recombinant Mesd protein (a specific inhibitor of LRP6) significantly decreased cell migration and invasion of TNBC MDA-MB-231 and BT549 cells. Interestingly, the effects of LRP6 knockdown and Mesd treatment on TNBC cell migration and invasion were more prominent than on TNBC cell proliferation/viability. Mechanistically, LRP6 knockdown and Mesd treatment inhibited Wnt/β-catenin signaling and decreased the expression of S100A4, a mediator of cancer metastasis and a specific target of Wnt/β-catenin signaling, in TNBC cells. Together, our data suggest that LRP6 promotes TNBC cell migration and invasion by regulating the expression and function of S100A4 via the Wnt/β-catenin signaling pathway. J. Cell. Biochem. 118: 2968-2976, 2017. © 2017 Wiley Periodicals, Inc.

摘要

低密度脂蛋白受体相关蛋白6（LRP6）是Wnt/β-连环蛋白信号通路中一种重要的Wnt共受体。尽管研究表明LRP6在多种癌症类型中表达增加，但其在肿瘤发生和进展中的功能仍有待阐明。我们在此证明，LRP6在人类三阴性乳腺癌（TNBC）患者和人类TNBC细胞系中表达上调，并且敲低LRP6表达以及用重组Mesd蛋白（LRP6的一种特异性抑制剂）处理显著降低了TNBC MDA-MB-231和BT549细胞的迁移和侵袭能力。有趣的是，敲低LRP6和Mesd处理对TNBC细胞迁移和侵袭的影响比对TNBC细胞增殖/活力的影响更显著。从机制上讲，敲低LRP6和Mesd处理抑制了Wnt/β-连环蛋白信号通路，并降低了TNBC细胞中S100A4的表达，S100A4是癌症转移的介质以及Wnt/β-连环蛋白信号通路的一个特异性靶点。总之，我们的数据表明，LRP6通过Wnt/β-连环蛋白信号通路调节S100A4的表达和功能，从而促进TNBC细胞的迁移和侵袭。《细胞生物化学杂志》118: 2968 - 2976, 2017年。© 2017威利期刊公司。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8388/10928515/34b221253033/nihms-1969526-f0006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8388/10928515/34b221253033/nihms-1969526-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8388/10928515/9ad5f470280d/nihms-1969526-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8388/10928515/a060236b42d1/nihms-1969526-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8388/10928515/d0009c1b4402/nihms-1969526-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8388/10928515/f282184a9e59/nihms-1969526-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8388/10928515/3535496416af/nihms-1969526-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8388/10928515/34b221253033/nihms-1969526-f0006.jpg

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Cyclin G2 inhibits epithelial-to-mesenchymal transition by disrupting Wnt/β-catenin signaling.细胞周期蛋白G2通过破坏Wnt/β-连环蛋白信号传导来抑制上皮-间质转化。
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Estrogen promotes the brain metastatic colonization of triple negative breast cancer cells via an astrocyte-mediated paracrine mechanism.雌激素通过星形胶质细胞介导的旁分泌机制促进三阴性乳腺癌细胞的脑转移定植。
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