ArticleCell adhesion & migration2016
CCN1 (CYR61) and CCN3 (NOV) signaling drives human trophoblast cells into senescence and stimulates migration properties.
Article in Cell adhesion & migration, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- The integrated developmental stress response (ISR-DASR) shift reveals a functional transition from cellular to stem cell organismal adaptation.Scientific reports · 2026Article
- CCN1-induced senescence and dysfunction of umbilical cord blood endothelial colony-forming cells in the pathogenesis of preeclampsia.Frontiers in endocrinology · 2026Article
- ROS-degradable hydrogel delivering LOXL2-LNPs rescues disc degeneration by synchronously suppressing cellular senescence and oxidative damage.Journal of nanobiotechnology · 2025Article
- FRMD6 determines the cell fate towards senescence: involvement of the Hippo-YAP-CCN3 axis.Cell death and differentiation · 2024Article
- Cellular communication network 1 promotes CASP2 mRNA expression but suppresses its protein translation in esophageal adenocarcinoma.Journal of cell communication and signaling · 2024Article
- Involvement of Matricellular Proteins in Cellular Senescence: Potential Therapeutic Targets for Age-Related Diseases.International journal of molecular sciences · 2024Review
- CCN1-Mediated Signaling in Placental Villous Tissues after SARS-CoV-2 Infection in Term Pregnant Women: Implications for Dysregulated Angiogenesis.Current issues in molecular biology · 2024Article
- Effects of Gestational Arsenic Exposures on Placental and Fetal Development in Mice: The Role ofEnvironmental health perspectives · 2023Article
- Decidualization of human endometrial stromal cells requires steroid receptor coactivator-3.Frontiers in reproductive health · 2022Article
- Effect of Maternal Obesity in Mice on IL-6 Levels and Placental Endothelial Cell Homeostasis.Nutrients · 2020Article
- CCN3 Signaling Is Differently Regulated in Placental Diseases Preeclampsia and Abnormally Invasive Placenta.Frontiers in endocrinology · 2020Article
- Molecular signatures for CCN1, p21 and p27 in progressive mantle cell lymphoma.Journal of cell communication and signaling · 2019Article
- Function of p21 (Cip1/Waf1/Cancers · 2019Article
- The m6A demethylase ALKBH5 controls trophoblast invasion at the maternal-fetal interface by regulating the stability ofTheranostics · 2019Article
- Biological functions and role of CCN1/Cyr61 in embryogenesis and tumorigenesis in the female reproductive system (Review).Molecular medicine reports · 2018Review
- Elucidating the Pathogenesis of Pre-eclampsia Using In Vitro Models of Spiral Uterine Artery Remodelling.Current hypertension reports · 2017Review
- Function and Hormonal Regulation of GATA3 in Human First Trimester Placentation.Biology of reproduction · 2016Article
- Notch: A multi-functional integrating system of microenvironmental signals.Developmental biology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During placental development, continuous invasion of trophoblasts into the maternal compartment depends on the support of proliferating extravillous trophoblasts (EVTs). Unlike tumor cells, EVTs escape from the cell cycle before invasion into the decidua and spiral arteries. This study focused on the regulation properties of glycosylated and non-glycosylated matricellular CCN1 and CCN3, primarily for proliferation control in the benign SGHPL-5 trophoblast cell line, which originates from the first-trimester placenta. Treating SGHPL-5 trophoblast cells with the glycosylated forms of recombinant CCN1 and CCN3 decreased cell proliferation by bringing about G0/G1 cell cycle arrest, which was accompanied by the upregulation of activated Notch-1 and its target gene p21. Interestingly, both CCN proteins increased senescence-associated β-galactosidase activity and the expression of the senescence marker p16. The migration capability of SGHPL-5 cells was mostly enhanced in response to CCN1 and CCN3, by the activation of FAK and Akt kinase but not by the activation of ERK1/2. In summary, both CCN proteins play a key role in regulating trophoblast cell differentiation by inducing senescence and enhancing migration properties. Reduced levels of CCN1 and CCN3, as found in early-onset preeclampsia, could contribute to a shift from invasive to proliferative EVTs and may explain their shallow invasion properties in this disease.
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