Cell Adhesion & Migration ( IF 3.2 ) Pub Date : 2020-01-20 , DOI: 10.1080/19336918.2019.1710024 Sonam Verma 1 , Amandeep Kaur Kang 1 , Rahul Pal 2 , Satish Kumar Gupta 1
ABSTRACT
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.
中文翻译:
BST2通过STAT1和AKT信号通路以及E-钙黏着蛋白的表达,调节HTR-8 / SVneo细胞侵袭时γ-干扰素依赖性的减少。
摘要
干扰素-γ(IFN-γ)下调滋养细胞入侵的机制需要进一步研究。用IFN-γ处理HTR-8 / SVneo细胞可导致其侵袭性降低,同时BST2表达增加。siRNA对BST2的沉默表明,在用IFN-γ处理后,BST2的侵袭和扩散显着增加,并且E-cadherin的表达下调。此外,STAT1沉默抑制BST2和E-钙黏着蛋白表达的IFN-γ依赖性增加。用IFN-γ处理HTR-8 / SVneo细胞可导致AKT活化,而PI3K抑制剂对它的抑制作用则消除了IFN-γ介导的侵袭/扩散减少以及BST2和E-钙粘蛋白表达下调。总的来说,