ArticleMolecular biology of the cell2012
Synemin promotes AKT-dependent glioblastoma cell proliferation by antagonizing PP2A.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
14 citing papers in PubMed, 34 citations in OpenAlex.
- Amino acid metabolism in glioblastoma pathogenesis, immune evasion, and treatment resistance.Cancer cell international · 2025Review
- Synemin promotes pulmonary artery smooth muscle cell phenotypic switch in shunt-induced pulmonary arterial hypertension.ESC heart failure · 2022Article
- TheToxins · 2022Article
- The Intermediate Filament Synemin Regulates Non-Homologous End Joining in an ATM-Dependent Manner.Cancers · 2020Article
- Synemin Redefined: Multiple Binding Partners Results in Multifunctionality.Frontiers in cell and developmental biology · 2020Review
- Review
- Rare Case of Ulnar-Mammary-Like Syndrome With Left Ventricular Tachycardia and Lack ofFrontiers in genetics · 2018Article
- Absence of synemin in mice causes structural and functional abnormalities in heart.Journal of molecular and cellular cardiology · 2018Article
- The cytoskeleton meets the skeleton. Focus on "Deficiency of the intermediate filament synemin reduces bone mass in vivo".American journal of physiology. Cell physiology · 2016Article
- Myopathic changes in murine skeletal muscle lacking synemin.American journal of physiology. Cell physiology · 2015Article
- GBA deficiency promotes SNCA/α-synuclein accumulation through autophagic inhibition by inactivated PPP2A.Autophagy · 2015Article
- Synemin: an evolving role in tumor growth and progression.Journal of cachexia, sarcopenia and muscle · 2014Article
- Review on intermediate filaments of the nervous system and their pathological alterations.Histochemistry and cell biology · 2013Review
- S100A8/A9 (calprotectin) negatively regulates G2/M cell cycle progression and growth of squamous cell carcinoma.PloS one · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The intermediate filament protein synemin is present in astrocyte progenitors and glioblastoma cells but not in mature astrocytes. Here we demonstrate a role for synemin in enhancing glioblastoma cell proliferation and clonogenic survival, as synemin RNA interference decreased both behaviors by inducing G1 arrest along with Rb hypophosphorylation and increased protein levels of the G1/S inhibitors p21(Cip1) and p27(Kip1). Akt involvement was demonstrated by decreased phosphorylation of its substrate, p21(Cip1), and reduced Akt catalytic activity and phosphorylation at essential activation sites. Synemin silencing, however, did not affect the activities of PDPK1 and mTOR complex 2, which directly phosphorylate Akt activation sites, but instead enhanced the activity of the major regulator of Akt dephosphorylation, protein phosphatase type 2A (PP2A). This was accompanied by changes in PP2A subcellular distribution resulting in increased physical interactions between PP2A and Akt, as shown by proximity ligation assays (PLAs). PLAs and immunoprecipitation experiments further revealed that synemin and PP2A form a protein complex. In addition, treatment of synemin-silenced cells with the PP2A inhibitor cantharidic acid resulted in proliferation and pAkt and pRb levels similar to those of controls. Collectively these results indicate that synemin positively regulates glioblastoma cell proliferation by helping sequester PP2A away from Akt, thereby favoring Akt activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.