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S100A6基因沉默对在位子宫内膜基质细胞生物学特性及β-连环蛋白表达的影响

Effects of S100A6 gene silencing on the biological features of eutopic endometrial stromal cells and β‑catenin expression.

作者信息

Zhang Xiaoling, Liu Zequn, Chen Meihong, Cao Qing, Huang Donghua

机构信息

Department of Gynecology, Jiangxi Maternal and Child Health Hospital, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.

Department of Medicine, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.

出版信息

Mol Med Rep. 2017 Mar;15(3):1279-1285. doi: 10.3892/mmr.2017.6105. Epub 2017 Jan 5.

Abstract

Protein expression levels of S100 calcium binding protein A6 (S100A6) are increased in various malignancies and are associated with tumor behavior; however, the association between S100A6 and endometriosis remains to be elucidated. In order to investigate the influence of S100A6 protein, recombinant lentivirus siS100A6 was used to transfect the eutopic endometrial stromal cells. CCK‑8 assay was performed to identify the proliferation ability of cell and the cell migration was detected by Transwell assay. Flow cytometry was performed to detect cell apoptosis, and western blotting and reverse transcription‑quantitative polymerase chain reaction were performed to identify the expression of β‑catenin. The present study investigated the role of S100A6 in endometriosis and its interaction with β‑catenin by transfecting eutopic endometrial stromal cells with a recombinant lentivirus containing S100A6‑specific small interfering RNA. Inhibition of S100A6 expression had a significant antiproliferative effect and reduced the migratory ability of eutopic endometrial stromal cells, and induced their apoptosis. In addition, inhibition of S100A6 expression suppressed β‑catenin expression. These results suggested that inhibition of S100A6 may represent a promising novel approach for the targeted therapy of endometriosis.

摘要

S100钙结合蛋白A6(S100A6)的蛋白表达水平在多种恶性肿瘤中升高,并与肿瘤行为相关;然而,S100A6与子宫内膜异位症之间的关联仍有待阐明。为了研究S100A6蛋白的影响,使用重组慢病毒siS100A6转染在位子宫内膜基质细胞。进行CCK-8检测以鉴定细胞的增殖能力,并通过Transwell检测法检测细胞迁移。进行流式细胞术检测细胞凋亡,并进行蛋白质印迹和逆转录-定量聚合酶链反应以鉴定β-连环蛋白的表达。本研究通过用含有S100A6特异性小干扰RNA的重组慢病毒转染在位子宫内膜基质细胞,研究了S100A6在子宫内膜异位症中的作用及其与β-连环蛋白的相互作用。抑制S100A6表达具有显著的抗增殖作用,并降低了在位子宫内膜基质细胞的迁移能力,并诱导其凋亡。此外,抑制S100A6表达可抑制β-连环蛋白的表达。这些结果表明,抑制S100A6可能是一种有前景的子宫内膜异位症靶向治疗新方法。

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