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通过调节……促进乳腺癌。

promotes breast cancer via regulating .

作者信息

Huang Meiling, Xiao Jingjing, Yan Changjiao, Wang Ting, Ling Rui

机构信息

Department of Thyroid, Breast, and Vascular Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.

出版信息

Ann Transl Med. 2021 Oct;9(20):1566. doi: 10.21037/atm-21-4921.

DOI:10.21037/atm-21-4921
PMID:34790772
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8576695/
Abstract

BACKGROUND

Breast cancer (BC) is the most common cancer diagnosed among women and is the second leading cause of cancer death. It is of great significance to explore potential candidate targets for BC.

METHODS

The expression of ubiquitin-specific protease 41 () and its prognosis prediction function was firstly evaluated by TCGA database analysis. Using BC cell lines and specimens from 10 patients with primary BC, the upregulation of in BC was ensured. By overexpression or knockdown, its function was studied by cell function assays, small interfering RNA (), western blot, mass spectrometry, and flow cytometry. The potential mechanism of was explored via Co-Immunoprecipitation mass spectrometry, and western blot.

RESULTS

TCGA database analysis revealed that in metastatic BC, expression was upregulated and negatively correlated with BC prognosis. In BC cancer cells and cancer specimens, was also upregulated. Overexpression of greatly enhanced BC colony-forming ability, proliferation, and migration. In contrast, knockdown significantly inhibited BC colony-forming ability, proliferation, and migration. Moreover, Co-Immunoprecipitation mass spectrometry results indicated that could interact with . promoted the protein expression of . The expression of in BC tissues was upregulated. Knockdown of inhibited cell growth and migration, and reversed the oncogenic function of in BC cells.

CONCLUSIONS

can be a potential therapeutic target against BC via .

摘要

背景

乳腺癌(BC)是女性中诊断出的最常见癌症,也是癌症死亡的第二大主要原因。探索BC的潜在候选靶点具有重要意义。

方法

首先通过TCGA数据库分析评估泛素特异性蛋白酶41()的表达及其预后预测功能。使用BC细胞系和10例原发性BC患者的标本,证实了BC中该蛋白的上调。通过过表达或敲低,通过细胞功能测定、小干扰RNA()、蛋白质印迹、质谱和流式细胞术研究其功能。通过免疫共沉淀质谱和蛋白质印迹探索其潜在机制。

结果

TCGA数据库分析显示,在转移性BC中,该蛋白表达上调且与BC预后呈负相关。在BC癌细胞和癌组织标本中,该蛋白也上调。该蛋白的过表达大大增强了BC的集落形成能力、增殖和迁移能力。相反,敲低该蛋白显著抑制了BC的集落形成能力、增殖和迁移能力。此外,免疫共沉淀质谱结果表明该蛋白可与相互作用。该蛋白促进了的蛋白表达。BC组织中该蛋白的表达上调。敲低该蛋白可抑制细胞生长和迁移,并逆转该蛋白在BC细胞中的致癌功能。

结论

该蛋白可通过成为针对BC的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/358cca2fb25e/atm-09-20-1566-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/76c08e797c65/atm-09-20-1566-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/7bdd76abdafe/atm-09-20-1566-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/ed8455af7467/atm-09-20-1566-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/7d55239e43da/atm-09-20-1566-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/5cea73df7275/atm-09-20-1566-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/4c77d802e90f/atm-09-20-1566-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/358cca2fb25e/atm-09-20-1566-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/76c08e797c65/atm-09-20-1566-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/7bdd76abdafe/atm-09-20-1566-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/ed8455af7467/atm-09-20-1566-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/7d55239e43da/atm-09-20-1566-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/5cea73df7275/atm-09-20-1566-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/4c77d802e90f/atm-09-20-1566-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644c/8576695/358cca2fb25e/atm-09-20-1566-f7.jpg

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