KISS-1 knockdown inhibits cell growth, migration, and invasion in HTR-8/SVneo cells by regulating the GRP54-mediated PI3K/AKT signaling pathway.

IF 3.3 4区医学 Q3 IMMUNOLOGY Autoimmunity Pub Date : 2024-12-01 Epub Date: 2023-12-28 DOI:10.1080/08916934.2023.2297564

Lingna Chen, Yuying Ruan, Liping Ni, Guiting Wang, Yajuan Gao, Jindi Zhang, Dingheng Li, Haiou Xu

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引用次数: 0

Abstract

Recurrent spontaneous abortions (RSA) affect reproductive health and increase the risk of subsequent abortions. To investigate the role of KISS-1/GPR-54 signaling in RSA progression. Villus tissue was collected from RSA patients, and human trophoblastic HTR-8/SVneo cells were used. KISS-1 and GRP54 levels were detected using RT-qPCR and immunohistochemistry. Western blotting was performed to analyze ZO-1 and ZEB1 levels. Cell proliferation was determined via CCK-8 and cell clone formation assays. Transwell assays were performed to assess cell migration and invasion abilities. KISS-1 was down-regulated in the villus tissues of RSA patients. KISS-1 overexpression dramatically inhibited trophoblast proliferation, migration, and invasion. Mechanistically, ZEB1 expression was down-regulated, whereas ZO-1 expression was up-regulated, after KISS-1 overexpression. GPR54 silencing neutralized the effect of KISS-1 in HTR-8/SVneo cells. Additionally, KISS-1 overexpression inactivated the PI3K/AKT signaling pathway through GRP54. The KISS-1/GPR-54 signaling axis regulates RSA progression by regulating the PI3K/AKT signaling pathway.

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通过调节 GRP54 介导的 PI3K/AKT 信号通路，敲除 KISS-1 可抑制 HTR-8/SVneo 细胞的生长、迁移和侵袭。

反复自然流产（RSA）会影响生殖健康并增加后续流产的风险。研究KISS-1/GPR-54信号在RSA进展中的作用。研究人员采集了 RSA 患者的绒毛组织，并使用了人类滋养细胞 HTR-8/SVneo 细胞。采用 RT-qPCR 和免疫组织化学方法检测 KISS-1 和 GRP54 的水平。用 Western 印迹法分析 ZO-1 和 ZEB1 的水平。通过 CCK-8 和细胞克隆形成试验确定细胞增殖。透孔试验用于评估细胞迁移和侵袭能力。在RSA患者的绒毛组织中，KISS-1被下调。KISS-1的过表达能显著抑制滋养细胞的增殖、迁移和侵袭。从机制上讲，KISS-1过表达后，ZEB1的表达下调，而ZO-1的表达上调。GPR54 沉默中和了 KISS-1 在 HTR-8/SVneo 细胞中的作用。此外，KISS-1 的过表达通过 GRP54 使 PI3K/AKT 信号通路失活。KISS-1/GPR-54信号轴通过调节PI3K/AKT信号通路来调控RSA的进展。

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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来源期刊

Autoimmunity 医学-免疫学

CiteScore

5.70

自引率

8.60%

发文量

审稿时长

6-12 weeks

期刊介绍： Autoimmunity is an international, peer reviewed journal that publishes articles on cell and molecular immunology, immunogenetics, molecular biology and autoimmunity. Current understanding of immunity and autoimmunity is being furthered by the progress in new molecular sciences that has recently been little short of spectacular. In addition to the basic elements and mechanisms of the immune system, Autoimmunity is interested in the cellular and molecular processes associated with systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome, type I diabetes, multiple sclerosis and other systemic and organ-specific autoimmune disorders. The journal reflects the immunology areas where scientific progress is most rapid. It is a valuable tool to basic and translational researchers in cell biology, genetics and molecular biology of immunity and autoimmunity.