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通过相互作用组分析鉴定核仁素作为乳腺癌中一种新型的AEG-1相互作用蛋白

Identification of Nucleolin as a Novel AEG-1-Interacting Protein in Breast Cancer via Interactome Profiling.

作者信息

Lee Seong-Jae, Choi Kyoung-Min, Bang Geul, Park Seo-Gyu, Kim Eun-Bi, Choi Jin-Woong, Chung Young-Ho, Kim Jinyoung, Lee Seok-Geun, Kim Eunjung, Kim Jae-Young

机构信息

Graduate School of Analytical Science and Technology (GRAST), Chungnam National University, Daejeon 34134, Korea.

Research Center for Bioconvergence Analysis, Korea Basic Science Institute (KBSI), Ochang 28119, Korea.

出版信息

Cancers (Basel). 2021 Jun 7;13(11):2842. doi: 10.3390/cancers13112842.

DOI:10.3390/cancers13112842
PMID:34200450
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8201222/
Abstract

Breast cancer is one of the most common malignant diseases worldwide. Astrocyte elevated gene-1 (AEG-1) is upregulated in breast cancer and regulates breast cancer cell proliferation and invasion. However, the molecular mechanisms by which AEG-1 promotes breast cancer have yet to be fully elucidated. In order to delineate the function of AEG-1 in breast cancer development, we mapped the AEG-1 interactome via affinity purification followed by LC-MS/MS. We identified nucleolin (NCL) as a novel AEG-1 interacting protein, and co-immunoprecipitation experiments validated the interaction between AEG-1 and NCL in breast cancer cells. The silencing of NCL markedly reduced not only migration/invasion, but also the proliferation induced by the ectopic expression of AEG-1. Further, we found that the ectopic expression of AEG-1 induced the tyrosine phosphorylation of c-Met, and NCL knockdown markedly reduced this AEG-1 mediated phosphorylation. Taken together, our report identifies NCL as a novel mediator of the oncogenic function of AEG-1, and suggests that c-Met could be associated with the oncogenic function of the AEG-1-NCL complex in the context of breast cancer.

摘要

乳腺癌是全球最常见的恶性疾病之一。星形胶质细胞上调基因1（AEG-1）在乳腺癌中上调，并调节乳腺癌细胞的增殖和侵袭。然而，AEG-1促进乳腺癌的分子机制尚未完全阐明。为了阐明AEG-1在乳腺癌发展中的功能，我们通过亲和纯化结合液相色谱-串联质谱（LC-MS/MS）绘制了AEG-1相互作用组。我们鉴定出核仁素（NCL）是一种新的与AEG-1相互作用的蛋白质，免疫共沉淀实验验证了乳腺癌细胞中AEG-1与NCL之间的相互作用。NCL的沉默不仅显著降低了迁移/侵袭，还降低了AEG-1异位表达诱导的增殖。此外，我们发现AEG-1的异位表达诱导了c-Met的酪氨酸磷酸化，而NCL敲低显著降低了这种AEG-1介导的磷酸化。综上所述，我们的报告鉴定出NCL是AEG-1致癌功能的一种新介质，并表明在乳腺癌背景下，c-Met可能与AEG-1-NCL复合物的致癌功能相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f37/8201222/f97e34d21574/cancers-13-02842-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f37/8201222/805c85259731/cancers-13-02842-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f37/8201222/33e20da52a20/cancers-13-02842-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f37/8201222/243bda2bd945/cancers-13-02842-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f37/8201222/f97e34d21574/cancers-13-02842-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f37/8201222/805c85259731/cancers-13-02842-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f37/8201222/33e20da52a20/cancers-13-02842-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f37/8201222/243bda2bd945/cancers-13-02842-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f37/8201222/f97e34d21574/cancers-13-02842-g004.jpg

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本文引用的文献

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Combinatorial Inhibition of Cell Surface Receptors Using Dual Aptamer-Functionalized Nanoconstructs for Cancer Treatment.
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