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

AbstractRecurrent 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 an...

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Main Authors: Lingna Chen, Yuying Ruan, Liping Ni, Guiting Wang, Yajuan Gao, Jindi Zhang, Dingheng Li, Haiou Xu
Format: Article
Language:English
Published: Taylor & Francis Group 2024-12-01
Series:Autoimmunity
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/08916934.2023.2297564
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author Lingna Chen
Yuying Ruan
Liping Ni
Guiting Wang
Yajuan Gao
Jindi Zhang
Dingheng Li
Haiou Xu
author_facet Lingna Chen
Yuying Ruan
Liping Ni
Guiting Wang
Yajuan Gao
Jindi Zhang
Dingheng Li
Haiou Xu
author_sort Lingna Chen
collection DOAJ
description AbstractRecurrent 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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spelling doaj.art-b9d2112cf4ef4b009c13595df4424a862023-12-29T06:13:14ZengTaylor & Francis GroupAutoimmunity0891-69341607-842X2024-12-0157110.1080/08916934.2023.2297564KISS-1 knockdown inhibits cell growth, migration, and invasion in HTR-8/SVneo cells by regulating the GRP54-mediated PI3K/AKT signaling pathwayLingna Chen0Yuying Ruan1Liping Ni2Guiting Wang3Yajuan Gao4Jindi Zhang5Dingheng Li6Haiou Xu7Hangzhou Women’s Hospital, Hangzhou, ChinaHangzhou Women’s Hospital, Hangzhou, ChinaHangzhou Women’s Hospital, Hangzhou, ChinaHangzhou Women’s Hospital, Hangzhou, ChinaHangzhou Women’s Hospital, Hangzhou, ChinaHangzhou Women’s Hospital, Hangzhou, ChinaHangzhou Women’s Hospital, Hangzhou, ChinaHangzhou Women’s Hospital, Hangzhou, ChinaAbstractRecurrent 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.https://www.tandfonline.com/doi/10.1080/08916934.2023.2297564Recurrent spontaneous abortionKISS-1GPR54PI3K/AKT
spellingShingle Lingna Chen
Yuying Ruan
Liping Ni
Guiting Wang
Yajuan Gao
Jindi Zhang
Dingheng Li
Haiou Xu
KISS-1 knockdown inhibits cell growth, migration, and invasion in HTR-8/SVneo cells by regulating the GRP54-mediated PI3K/AKT signaling pathway
Autoimmunity
Recurrent spontaneous abortion
KISS-1
GPR54
PI3K/AKT
title KISS-1 knockdown inhibits cell growth, migration, and invasion in HTR-8/SVneo cells by regulating the GRP54-mediated PI3K/AKT signaling pathway
title_full KISS-1 knockdown inhibits cell growth, migration, and invasion in HTR-8/SVneo cells by regulating the GRP54-mediated PI3K/AKT signaling pathway
title_fullStr KISS-1 knockdown inhibits cell growth, migration, and invasion in HTR-8/SVneo cells by regulating the GRP54-mediated PI3K/AKT signaling pathway
title_full_unstemmed KISS-1 knockdown inhibits cell growth, migration, and invasion in HTR-8/SVneo cells by regulating the GRP54-mediated PI3K/AKT signaling pathway
title_short KISS-1 knockdown inhibits cell growth, migration, and invasion in HTR-8/SVneo cells by regulating the GRP54-mediated PI3K/AKT signaling pathway
title_sort kiss 1 knockdown inhibits cell growth migration and invasion in htr 8 svneo cells by regulating the grp54 mediated pi3k akt signaling pathway
topic Recurrent spontaneous abortion
KISS-1
GPR54
PI3K/AKT
url https://www.tandfonline.com/doi/10.1080/08916934.2023.2297564
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