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洛伐他汀对MDA-MB-231乳腺癌细胞的影响:抗体微阵列分析

Effects of Lovastatin on MDA-MB-231 Breast Cancer Cells: An Antibody Microarray Analysis.

作者信息

Yang Tao, Yao Hui, He Guangchun, Song Liujiang, Liu Ning, Wang Yan, Yang Yingke, Keller Evan T, Deng Xiyun

机构信息

1. National Engineering Laboratory for Rice and Byproduct Deep Processing, Central South University of Forestry and Technology, Changsha, Hunan 410004, China;

2. Medical College, Hunan Normal University, Changsha, Hunan 410013, China;

出版信息

J Cancer. 2016 Jan 1;7(2):192-9. doi: 10.7150/jca.13414. eCollection 2016.

DOI:10.7150/jca.13414
PMID:26819643
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4716852/
Abstract

Despite the tremendous improvement in cancer therapeutics, treatment of late-stage breast cancer remains a challenge for both basic scientists and clinicians. Lovastatin, a natural product derived from Aspergillus terreus or Monascus ruber, has been widely used as cholesterol-lowing drug in the clinic. It also has anti-cancer properties through poorly defined molecular mechanisms. In the present study, we employed a novel antibody microarray technology to investigate the molecular mechanisms through which lovastatin inhibits breast cancer. We found that lovastatin up-regulated 17 proteins and down-regulated 20 proteins in MDA-MB-231 breast cancer cells. These included proteins that modulate apoptosis, cell proliferation, differentiation, signal transduction, epithelial-to-mesenchymal transition and tumor metastasis. Modulation of these pathways may mediate, in part, the inhibitory activity of lovastatin on breast cancer.

摘要

尽管癌症治疗取得了巨大进步,但晚期乳腺癌的治疗对基础科学家和临床医生来说仍是一项挑战。洛伐他汀是一种从土曲霉或红曲霉菌中提取的天然产物,在临床上已被广泛用作降胆固醇药物。它还通过尚不明确的分子机制具有抗癌特性。在本研究中,我们采用了一种新型抗体微阵列技术来研究洛伐他汀抑制乳腺癌的分子机制。我们发现,洛伐他汀使MDA-MB-231乳腺癌细胞中的17种蛋白质上调,20种蛋白质下调。这些蛋白质包括调节细胞凋亡、细胞增殖、分化、信号转导、上皮-间质转化和肿瘤转移的蛋白质。这些途径的调节可能部分介导了洛伐他汀对乳腺癌的抑制活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/4716852/2a47bd23350a/jcav07p0192g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/4716852/cd6e4405538e/jcav07p0192g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/4716852/fa9dd32ff21c/jcav07p0192g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/4716852/b25e7d45bc0b/jcav07p0192g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/4716852/2a47bd23350a/jcav07p0192g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/4716852/cd6e4405538e/jcav07p0192g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/4716852/fa9dd32ff21c/jcav07p0192g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/4716852/b25e7d45bc0b/jcav07p0192g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/4716852/2a47bd23350a/jcav07p0192g004.jpg

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TGF-β Induces Degradation of PTHrP Through Ubiquitin-Proteasome System in Hepatocellular Carcinoma.转化生长因子-β通过泛素-蛋白酶体系统诱导甲状旁腺激素相关蛋白在肝癌中的降解。
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