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Keywords {🔍}

pubmed, article, google, scholar, cas, autophagy, central, cell, rhabdomyosarcoma, cancer, cells, alveolar, staufen, biol, muscle, mol, regulation, stau, skeletal, ravelchapuis, jasmin, ottawa, data, protein, jnk, signaling, wang, cellular, parks, expression, rna, med, almasi, crawford, côté, survival, arms, promotes, apoptosis, inhibition, human, sci, research, rnabinding, effect, access, zhang, liu, pathway, mtor,

Topics {✒️}

activating p38‐nuclear factor‐kappa hif-1α/beclin1-mediated autophagy month download article/chapter rna-binding protein staufen1 complex protein-protein partnerships pubmed  google scholar article  google scholar real-time quantitative pcr trpm2 channel-mediated regulation cisplatin-resistant osteosarcoma cells ros-mediated cellular signaling phospho-akt p-jnk reactive oxygen species phospho-mtor p-akt c-myc–dependent mechanism pax3/7-foxo1-induced tumorigenesis ros/jnk signaling pathway hsmm-c3 cell lines rna binding protein skeletal muscle cells related subjects skeletal muscle tumors oridonin-induced apoptosis independent events dm1 skeletal muscle stau1-overexpressing transgenic mice rna-binding proteins rna binding proteins ciclopirox induces autophagy jnk-signaling pathway jnk signaling pathway human osteosarcoma cells detachment-induced autophagy privacy choices/manage cookies autophagy gene transcripts full article pdf autophagy-related proteins 5 human chondrosarcoma cells aloe emodin inhibits google scholar c-myc-dependent cellular stress responses animal care guidelines skeletal muscles obtained essential degradation program tumor necrosis factor mtor-dependent manner muscle-specific expression osteosarcoma mg63 cells cancer research society

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• Winton, mTOR regulation by JNK: rescuing the starving intestinal cancer cell?

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         headline:Differential regulation of autophagy by STAU1 in alveolar rhabdomyosarcoma and non‐transformed skeletal muscle cells
         description:Recent work has highlighted the therapeutic potential of targeting autophagy to modulate cell survival in a variety of diseases including cancer. Recently, we found that the RNA-binding protein Staufen1 (STAU1) is highly expressed in alveolar rhabdomyosarcoma (ARMS) and that this abnormal expression promotes tumorigenesis. Here, we asked whether STAU1 is involved in the regulation of autophagy in ARMS cells. We assessed the impact of STAU1 expression modulation in ARMS cell lines (RH30 and RH41), non-transformed skeletal muscle cells (C2C12) and STAU1-transgenic mice using complementary techniques. We found that STAU1 silencing reduces autophagy in the ARMS cell lines RH30 and RH41, while increasing their apoptosis. Mechanistically, this inhibitory effect was found to be caused by a direct negative impact of STAU1 depletion on the stability of Beclin-1 (BECN1) and ATG16L1 mRNAs, as well as by an indirect inhibition of JNK signaling via increased expression of Dual specificity phosphatase 8 (DUSP8). Pharmacological activation of JNK or expression silencing of DUSP8 was sufficient to restore autophagy in STAU1-depleted cells. By contrast, we found that STAU1 downregulation in non-transformed skeletal muscle cells activates autophagy in a mTOR-dependent manner, without promoting apoptosis. A similar effect was observed in skeletal muscles obtained from STAU1-overexpressing transgenic mice. Together, our data indicate an effect of STAU1 on autophagy regulation in ARMS cells and its differential role in non-transformed skeletal muscle cells. Our findings suggest a cancer-specific potential of targeting STAU1 for the treatment of ARMS.
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            address:
               name:Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Canada
               type:PostalAddress
            type:Organization
            name:University of Ottawa
            address:
               name:The Eric J. Poulin Centre for Neuromuscular Diseases, Faculty of Medicine, University of Ottawa, Ottawa, Canada
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Canada
      name:The Eric J. Poulin Centre for Neuromuscular Diseases, Faculty of Medicine, University of Ottawa, Ottawa, Canada
      name:Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Canada
      name:The Eric J. Poulin Centre for Neuromuscular Diseases, Faculty of Medicine, University of Ottawa, Ottawa, Canada
      name:Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Canada
      name:The Eric J. Poulin Centre for Neuromuscular Diseases, Faculty of Medicine, University of Ottawa, Ottawa, Canada
      name:Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Canada
      name:The Eric J. Poulin Centre for Neuromuscular Diseases, Faculty of Medicine, University of Ottawa, Ottawa, Canada
      name:Division of Endocrinology, Department of Paediatric, CHEO, University of Ottawa, Ottawa, Canada
      name:Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Canada
      name:The Eric J. Poulin Centre for Neuromuscular Diseases, Faculty of Medicine, University of Ottawa, Ottawa, Canada
      name:Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Canada
      name:Division of Paediatric Surgery, Department of Surgery, CHEO, University of Ottawa, Ottawa, Canada
      name:Molecular Biomedicine Program, CHEO, Ottawa, Canada
      name:Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Canada
      name:The Eric J. Poulin Centre for Neuromuscular Diseases, Faculty of Medicine, University of Ottawa, Ottawa, Canada
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