ArticleFrontiers in cell and developmental biology2021
STX2 Promotes Trophoblast Growth, Migration, and Invasion Through Activation of the PI3K-AKT Pathway in Preeclampsia.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- UBE3A Inhibits Trophoblast Cell Migration and Invasion by Promoting ITGB1 Degradation and Affecting PI3K/AKT Signaling.The Kaohsiung journal of medical sciences · 2026Article
- Regulation of PI3K/Akt in preeclampsia: an examination of its pathological role and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Autophagy in PE: Dispute, Role and Potential Target.Cell proliferation · 2025Review
- Deciphering Shared Gene Signatures and Immune Infiltration Characteristics Between Gestational Diabetes Mellitus and Preeclampsia by Integrated Bioinformatics Analysis and Machine Learning.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Differential mRNA and lncRNA Expression Profiles Associated with Early Pregnancy Loss in ART Patients.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Circular RNA circ_0022707 impedes the progression of preeclampsia via the miR-3135b/GHR/PI3K/Akt axis.Functional & integrative genomics · 2024Article
- LMWH prevents thromboinflammation in the placenta via HBEGF-AKT signaling.Blood advances · 2024Article
- Potential molecular mechanisms and clinical implications of piRNAs in preeclampsia: a review.Reproductive biology and endocrinology : RB&E · 2024Review
- Bioinformatic Analysis Identifies Potential Extracellular Matrix Related Genes in the Pathogenesis of Early Onset Preeclampsia.Biochemical genetics · 2024Article
- Unraveling the molecular mechanisms driving enhanced invasion capability of extravillous trophoblast cells: a comprehensive review.Journal of assisted reproduction and genetics · 2024Review
- Upregulation of SEMP1 Contributes to Improving the Biological Functions of Trophoblast via the PI3K/AKT Pathway in Preeclampsia.Molecular biotechnology · 2024Article
- Mechanism of histone deacetylase HDAC2 in FOXO3-mediated trophoblast pyroptosis in preeclampsia.Functional & integrative genomics · 2023Article
- LncRNA LINC00534 regulates cell proliferation and migration via the miR-494-3p/PTEN axis in HTR-8/SVneo cells.Journal of clinical laboratory analysis · 2023Article
- Article
- SNHG22 promotes migration and invasion of trophoblasts via miR-128-3p/PCDH11X axis and activates PI3K/Akt signaling pathway.Clinics (Sao Paulo, Brazil) · 2022Article
- FPR2 serves a role in recurrent spontaneous abortion by regulating trophoblast function via the PI3K/AKT signaling pathway.Molecular medicine reports · 2021Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesAbnormal trophoblast behaviors during pregnancy contribute to the development of preeclampsia (PE). Syntaxin2 (STX2) has been shown to be a crucial epithelial mediator in numerous diseases. However, the functions of STX2 and the mechanisms underlying its role in PE remain largely unknown. The aim of this study was to explore the role of STX2 on trophoblast biology and unravel the molecular mechanisms that contribute to the development and progression of PE. MATERIALS AND
methodsWe first compared the expression of STX2 in placental tissues from women with PE and women with normal pregnancies. Then, we investigated the role of STX2 on trophoblast proliferation, migration and invasion in HTR-8/SVneo and primary human trophoblast cells by loss or gain of function experiments. In addition, co-immunoprecipitation, pulldown and immunofluorescence assays were performed to investigate the co-localization of STX2 with other proteins, and to help clarify the mechanisms underlying STX2-mediated functions on trophoblasts.
resultsWe demonstrated that STX2 expression was downregulated in placental tissues of women with PE compared with those from normal pregnancies. Loss and gain of function experiments further confirmed a role for STX2 in cell proliferation, migration and invasion in trophoblasts. By co-immunoprecipitation, pulldown and immunofluorescence co-localization assays, we revealed that STX2 selectively interacted with p85, a subunit of PI3K, and directly recruited p85 to the cytomembrane, thereby activating the AKT signaling pathway. We further demonstrated that the AKT activation was abolished by the use of a PI3K inhibitor (LY294002), which negatively affected STX2-mediated functions on trophoblasts.
conclusionAll together, our findings point to a crucial role for STX2 in PE progression. Our new insights also suggest that STX2 may be a potential diagnostic tool and a novel therapeutic target for treating PE.
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