ArticleCell communication and signaling : CCS2020
Presenilin1 exerts antiproliferative effects by repressing the Wnt/β-catenin pathway in glioblastoma.
Article in Cell communication and signaling : CCS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- IFIT3-DVL interaction promotes malignant progression of lung squamous cell carcinoma and large-cell lung carcinoma via canonical WNT signaling.The Journal of biological chemistry · 2026Article
- The preliminary study on the effect of PSEN1 on the proliferation and invasion of breast cancer cells.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2026Article
- Pharmacological inhibition of RE1 silencing transcription factor disrupts SOX2 expression and neurogenesis in human induced pluripotent stem cells derived neuronal models.Metabolic brain disease · 2025Article
- MicroRNAs: pioneering regulators in Alzheimer's disease pathogenesis, diagnosis, and therapy.Translational psychiatry · 2024Review
- Yttrium oxide nanoparticles ameliorates calcium hydroxide and calcium titanate nanoparticles induced genomic DNA and mitochondrial damage, ROS generation and inflammation.Scientific reports · 2024Article
- Article
- Presenilin-1 (PSEN1) Mutations: Clinical Phenotypes beyond Alzheimer's Disease.International journal of molecular sciences · 2023Review
- The critical role of γ-secretase and its inhibitors in cancer and cancer therapeutics.International journal of biological sciences · 2023Review
- Estimation of genotoxicity, apoptosis and oxidative stress induction by TiOScientific reports · 2022Article
- Activating transcription factor 2 promotes the progression of hepatocellular carcinoma by inducing the activation of the WHSC1-mediated TOP2A/PI3K/AKT axis.The Kaohsiung journal of medical sciences · 2022Article
- Role of Presenilin-1 in Aggressive Human Melanoma.International journal of molecular sciences · 2022Article
- Presenilin1 inhibits glioblastoma cell invasiveness via promoting Sortilin cleavage.Cell communication and signaling : CCS · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
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Abstract
backgroundGlioblastoma and Alzheimer's disease (AD) are the most common and devastating diseases in the central nervous system. The dysfunction of Presenilin1 is the main reason for AD pathogenesis. However, the molecular function of Presenilin1 and its relative mechanism in glioblastoma remain unclear.
methodsExpression of presenilin1 in glioma was determined by IHC. CCK-8, colony formation, Flow cytometry, Edu staining were utilized to evaluate functions of presenilin1 on glioblastoma proliferation. The mechanism of above process was assessed by Western blotting and cell immunofluorescence. Mouse transplanting glioblastoma model and micro-MRI detection were used to verified presenilin1 function in vivo.
resultsIn this study, we found that all grades of glioma maintained relatively low Presenilin1 expression and that the expression of Presenilin1 in high-grade glioma was significantly lower than that in low-grade glioma. Moreover, the Presenilin1 level had a positive correlation with glioma and glioblastoma patient prognosis. Next, we determined that Presenilin1 inhibited the growth and proliferation of glioblastoma cells by downregulating CDK6, C-myc and Cyclin D1 to arrest the cell cycle at the G1/S phase. Mechanistically, Presenilin1 promoted the direct phosphorylation of β-catenin at the 45 site and indirect phosphorylation at the 33/37/41 site, then decreased the stabilized part of β-catenin and hindered its translocation from the cytoplasm to the nucleus. Furthermore, we found that Presenilin1 downregulation clearly accelerated the growth of subcutaneous glioblastoma, and Presenilin1 overexpression significantly repressed the subcutaneous and intracranial transplantation of glioblastoma by hindering β-catenin-dependent cell proliferation.
conclusionOur data implicate the antiproliferative effect of Presenilin1 in glioblastoma by suppressing Wnt/β-catenin signaling, which may provide a novel therapeutic agent for glioblastoma. Video Abstract.
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