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We began analyzing https://link.springer.com/article/10.1007/s00018-023-04969-4, but it redirected us to https://link.springer.com/article/10.1007/s00018-023-04969-4. The analysis below is for the second page.

Title[redir]:
Staufen1 controls mitochondrial metabolism via HIF2α in embryonal rhabdomyosarcoma and promotes tumorigenesis | Cellular and Molecular Life Sciences
Description:
Elevated mitochondrial metabolism promotes tumorigenesis of Embryonal Rhabdomyosarcomas (ERMS). Accordingly, targeting oxidative phosphorylation (OXPHOS) could represent a therapeutic strategy for ERMS. We previously demonstrated that genetic reduction of Staufen1 (STAU1) levels results in the inhibition of ERMS tumorigenicity. Here, we examined STAU1-mediated mechanisms in ERMS and focused on its potential involvement in regulating OXPHOS. We report the novel and differential role of STAU1 in mitochondrial metabolism in cancerous versus non-malignant skeletal muscle cells (NMSkMCs). Specifically, our data show that STAU1 depletion reduces OXPHOS and inhibits proliferation of ERMS cells. Our findings further reveal the binding of STAU1 to several OXPHOS mRNAs which affects their stability. Indeed, STAU1 depletion reduced the stability of OXPHOS mRNAs, causing inhibition of mitochondrial metabolism. In parallel, STAU1 depletion impacted negatively the HIF2α pathway which further modulates mitochondrial metabolism. Exogenous expression of HIF2α in STAU1-depleted cells reversed the mitochondrial inhibition and induced cell proliferation. However, opposite effects were observed in NMSkMCs. Altogether, these findings revealed the impact of STAU1 in the regulation of mitochondrial OXPHOS in cancer cells as well as its differential role in NMSkMCs. Overall, our results highlight the therapeutic potential of targeting STAU1 as a novel approach for inhibiting mitochondrial metabolism in ERMS.

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🏙️ Massive Traffic: 50M - 100M visitors per month


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Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Doi.org has a revenue plan, but it's either invisible or we haven't found it.

Keywords {🔍}

pubmed, article, google, scholar, cas, central, cell, mitochondrial, cancer, rhabdomyosarcoma, stau, metabolism, mol, staufen, cells, sci, ottawa, hifα, oxphos, mrna, data, embryonal, promotes, human, almasi, httpsdoiorgs, research, jasmin, erms, expression, access, res, nat, death, university, authors, canada, privacy, cookies, content, analysis, information, cellular, molecular, life, manuscript, kyle, oxidative, inhibition, skeletal,

Topics {✒️}

crawford parks te month download article/chapter hypoxia-inducible factor signalling hypoxia-inducible factor-2alpha jnj-26481585-induced antitumor activity trpm2 channel-mediated regulation stau1-mediated mrna decay replication-competent retroviruses abrogates examined stau1-mediated mechanisms staufen-mediated mrna decay mapk/erk signaling pathway hsmm-c3 cell lines stau1-depleted cells reversed hypoxia inducible factor rna-binding protein staufen1 full article pdf mitochondrial oxphos functions human transformed cells bonnet-magnaval stau1-mediated decay hypoxic tumour growth modulates mitochondrial metabolism inhibiting mitochondrial metabolism article almasi mitochondrial o2 consumption inhibits malignant progression cancer research society mitochondrial oxidative metabolism privacy choices/manage cookies article number 328 related subjects pediatr blood cancer key cellular events davis rj pabpc1-induced stabilization protein-protein interactions breast cancer cells mitochondrial oxphos biogenesis jnk-signaling pathway cell-cycle transitions mitochondrial respiratory complex stau1 depletion reduced solid cancer therapy induced cell proliferation mitochondrial oxidative stress article cellular foster mrna synthesis targeting hif-2α providing hsmm-c2 article log

Schema {🗺️}

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         headline:Staufen1 controls mitochondrial metabolism via HIF2α in embryonal rhabdomyosarcoma and promotes tumorigenesis
         description:Elevated mitochondrial metabolism promotes tumorigenesis of Embryonal Rhabdomyosarcomas (ERMS). Accordingly, targeting oxidative phosphorylation (OXPHOS) could represent a therapeutic strategy for ERMS. We previously demonstrated that genetic reduction of Staufen1 (STAU1) levels results in the inhibition of ERMS tumorigenicity. Here, we examined STAU1-mediated mechanisms in ERMS and focused on its potential involvement in regulating OXPHOS. We report the novel and differential role of STAU1 in mitochondrial metabolism in cancerous versus non-malignant skeletal muscle cells (NMSkMCs). Specifically, our data show that STAU1 depletion reduces OXPHOS and inhibits proliferation of ERMS cells. Our findings further reveal the binding of STAU1 to several OXPHOS mRNAs which affects their stability. Indeed, STAU1 depletion reduced the stability of OXPHOS mRNAs, causing inhibition of mitochondrial metabolism. In parallel, STAU1 depletion impacted negatively the HIF2α pathway which further modulates mitochondrial metabolism. Exogenous expression of HIF2α in STAU1-depleted cells reversed the mitochondrial inhibition and induced cell proliferation. However, opposite effects were observed in NMSkMCs. Altogether, these findings revealed the impact of STAU1 in the regulation of mitochondrial OXPHOS in cancer cells as well as its differential role in NMSkMCs. Overall, our results highlight the therapeutic potential of targeting STAU1 as a novel approach for inhibiting mitochondrial metabolism in ERMS.
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      headline:Staufen1 controls mitochondrial metabolism via HIF2α in embryonal rhabdomyosarcoma and promotes tumorigenesis
      description:Elevated mitochondrial metabolism promotes tumorigenesis of Embryonal Rhabdomyosarcomas (ERMS). Accordingly, targeting oxidative phosphorylation (OXPHOS) could represent a therapeutic strategy for ERMS. We previously demonstrated that genetic reduction of Staufen1 (STAU1) levels results in the inhibition of ERMS tumorigenicity. Here, we examined STAU1-mediated mechanisms in ERMS and focused on its potential involvement in regulating OXPHOS. We report the novel and differential role of STAU1 in mitochondrial metabolism in cancerous versus non-malignant skeletal muscle cells (NMSkMCs). Specifically, our data show that STAU1 depletion reduces OXPHOS and inhibits proliferation of ERMS cells. Our findings further reveal the binding of STAU1 to several OXPHOS mRNAs which affects their stability. Indeed, STAU1 depletion reduced the stability of OXPHOS mRNAs, causing inhibition of mitochondrial metabolism. In parallel, STAU1 depletion impacted negatively the HIF2α pathway which further modulates mitochondrial metabolism. Exogenous expression of HIF2α in STAU1-depleted cells reversed the mitochondrial inhibition and induced cell proliferation. However, opposite effects were observed in NMSkMCs. Altogether, these findings revealed the impact of STAU1 in the regulation of mitochondrial OXPHOS in cancer cells as well as its differential role in NMSkMCs. Overall, our results highlight the therapeutic potential of targeting STAU1 as a novel approach for inhibiting mitochondrial metabolism in ERMS.
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      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:Department of Surgery, Division of Paediatric Surgery, University of Ottawa, Children’s Hospital of Eastern Ontario, Ottawa, Canada
      name:Molecular Biomedicine Program, Children’s Hospital of Eastern Ontario, 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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