BST2通过STAT1和AKT信号通路以及E-cadherin的表达调控干扰素γ依赖性的HTR-8/SVneo细胞侵袭减少。

IF 3.3 3区 生物学 Q3 CELL BIOLOGY Cell Adhesion & Migration Pub Date : 2020-12-01 DOI:10.1080/19336918.2019.1710024
Sonam Verma, Amandeep Kaur Kang, Rahul Pal, Satish Kumar Gupta
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引用次数: 7

摘要

干扰素γ (IFN-γ)下调滋养细胞侵袭的机制有待进一步研究。用IFN-γ治疗HTR-8/SVneo细胞导致其侵袭减少,同时BST2表达增加。siRNA沉默BST2后,IFN-γ处理后BST2的侵袭和扩散显著增加,E-cadherin表达下调。此外,STAT1沉默抑制IFN-γ依赖性BST2和E-cadherin表达的增加。IFN-γ处理HTR-8/SVneo细胞可激活AKT, PI3K抑制剂抑制AKT可消除IFN-γ介导的侵袭/扩散减少,下调BST2和E-cadherin表达。综上所述,IFN-γ通过增加BST2和E-cadherin的表达,激活STAT1和AKT,从而降低HTR-8/SVneo细胞的侵袭。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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BST2 regulates interferon gamma-dependent decrease in invasion of HTR-8/SVneo cells via STAT1 and AKT signaling pathways and expression of E-cadherin.

The mechanism by which interferon-gamma (IFN-γ) downregulates trophoblast invasion needs further investigation. Treatment of HTR-8/SVneo cells with IFN-γ led to a decrease in their invasion concomitant with an increased expression of BST2. Silencing of BST2 by siRNA showed a significant increase in their invasion and spreading after treatment with IFN-γ as well as downregulated expression of E-cadherin. Further, STAT1 silencing inhibited the IFN-γ-dependent increase in the expression of BST2 and E-cadherin. Treatment of HTR-8/SVneo cells with IFN-γ led to the activation of AKT, and its inhibition with PI3K inhibitor abrogated IFN-γ-mediated decrease in invasion/spreading and downregulated BST2 and E-cadherin expression. Collectively, IFN-γ decreases the invasion of HTR-8/SVneo cells by STAT1 and AKT activation via increased expression of BST2 and E-cadherin.

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来源期刊
CiteScore
6.40
自引率
0.00%
发文量
7
审稿时长
53 weeks
期刊介绍: Cell Adhesion & Migration is a multi-disciplinary, peer reviewed open access journal that focuses on the biological or pathological implications of cell-cell and cell-microenvironment interactions. The main focus of this journal is fundamental science. The journal strives to serve a broad readership by regularly publishing review articles covering specific disciplines within the field, and by publishing focused issues that provide an overview on specific topics of interest within the field. Cell Adhesion & Migration publishes relevant and timely original research, as well as authoritative overviews, commentaries, and perspectives, providing context for the work presented in Cell Adhesion & Migration and for key results published elsewhere. Original research papers may cover all topics important in the field of cell-cell and cell-matrix interactions. Cell Adhesion & Migration also publishes articles related to cell biomechanics, biomaterial, and development of related imaging technologies.
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