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HSPC159 通过诱导上皮-间充质转化和激活 PI3K/Akt 通路促进乳腺癌的增殖和转移。

HSPC159 promotes proliferation and metastasis by inducing epithelial-mesenchymal transition and activating the PI3K/Akt pathway in breast cancer.

机构信息

Department of Diagnostic Pathology, Weifang Medical University, Weifang, China.

Key Lab of Neurological Disease and Regeneration&Repair, Weifang Medical University, Weifang, China.

出版信息

Cancer Sci. 2018 Jul;109(7):2153-2163. doi: 10.1111/cas.13631. Epub 2018 Jun 9.

DOI:10.1111/cas.13631
PMID:29737572
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6029831/
Abstract

HSPC159 is a novel human galectin-related protein that has been shown to be involved in carcinogenesis. Little is known about HSPC159 expression and function in breast cancer. Herein we showed that HSPC159 was aberrantly expressed in both breast cancer cell lines and tumor tissues and that its expression was associated with poor prognosis of breast cancer patients. Using gain- and loss-of-function methods we found that HSPC159 enhanced breast cancer cell proliferation and metastasis in vitro and in vivo. Mechanistically, HSPC159 was found to induce epithelial-mesenchymal transition (EMT) and the F-actin polymerization process of breast cancer cells. Moreover, HSPC159 promoted proliferation, migration and invasion through activating the PI3K/Akt signaling pathway in breast cancer. In conclusion, our findings showed that HSPC159 contributed to breast cancer progression through the PI3K/Akt pathway and might serve as a potential therapeutic target for the treatment of breast cancer.

摘要

HSPC159 是一种新型的人类半乳糖凝集素相关蛋白,已被证明参与了癌症的发生。关于 HSPC159 在乳腺癌中的表达和功能知之甚少。在此,我们发现 HSPC159 在乳腺癌细胞系和肿瘤组织中异常表达,其表达与乳腺癌患者的预后不良相关。通过功能获得和功能丧失方法,我们发现 HSPC159 增强了乳腺癌细胞在体外和体内的增殖和转移。机制上,发现 HSPC159 诱导乳腺癌细胞发生上皮-间充质转化(EMT)和 F-肌动蛋白聚合过程。此外,HSPC159 通过激活乳腺癌中的 PI3K/Akt 信号通路促进增殖、迁移和侵袭。总之,我们的研究结果表明,HSPC159 通过 PI3K/Akt 通路促进乳腺癌的进展,可能成为治疗乳腺癌的潜在治疗靶点。

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