We are analyzing https://link.springer.com/article/10.1186/s12885-016-2850-8.

Title:
Induction of autophagy by ARHI (DIRAS3) alters fundamental metabolic pathways in ovarian cancer models | BMC Cancer
Description:
Background Autophagy is a bulk catabolic process that modulates tumorigenesis, therapeutic resistance, and dormancy. The tumor suppressor ARHI (DIRAS3) is a potent inducer of autophagy and its expression results in necroptotic cell death in vitro and tumor dormancy in vivo. ARHI is down-regulated or lost in over 60 % of primary ovarian tumors yet is dramatically up-regulated in metastatic disease. The metabolic changes that occur during ARHI induction and their role in modulating death and dormancy are unknown. Methods We employed Nuclear Magnetic Resonance (NMR)-based metabolomic strategies to characterize changes in key metabolic pathways in both cell culture and xenograft models of ARHI expression and autophagy. These pathways were further interrogated by cell-based immunofluorescence imaging, tracer uptake studies, targeted metabolic inhibition, and in vivo PET/CT imaging. Results Induction of ARHI in cell culture models resulted in an autophagy-dependent increase in lactate production along with increased glucose uptake and enhanced sensitivity to glycolytic inhibitors. Increased uptake of glutamine was also dependent on autophagy and dramatically sensitized cultured ARHI-expressing ovarian cancer cell lines to glutaminase inhibition. Induction of ARHI resulted in a reduction in mitochondrial respiration, decreased mitochondrial membrane potential, and decreased Tom20 staining suggesting an ARHI-dependent loss of mitochondrial function. ARHI induction in mouse xenograft models resulted in an increase in free amino acids, a transient increase in [18F]-FDG uptake, and significantly altered choline metabolism. Conclusions ARHI expression has previously been shown to trigger autophagy-associated necroptosis in cell culture. In this study, we have demonstrated that ARHI expression results in decreased cellular ATP/ADP, increased oxidative stress, and decreased mitochondrial function. While this bioenergetic shock is consistent with programmed necrosis, our data indicates that the accompanying up-regulation of glycolysis and glutaminolysis is autophagy-dependent and serves to support cell viability rather than facilitate necroptotic cell death. While the mechanistic basis for metabolic up-regulation following ARHI induction is unknown, our preliminary data suggest that decreased mitochondrial function and increased metabolic demand may play a role. These alterations in fundamental metabolic pathways during autophagy-associated necroptosis may provide the basis for new therapeutic strategies for the treatment of dormant ovarian tumors.
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Topics {✒️}

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         description:Autophagy is a bulk catabolic process that modulates tumorigenesis, therapeutic resistance, and dormancy. The tumor suppressor ARHI (DIRAS3) is a potent inducer of autophagy and its expression results in necroptotic cell death in vitro and tumor dormancy in vivo. ARHI is down-regulated or lost in over 60 % of primary ovarian tumors yet is dramatically up-regulated in metastatic disease. The metabolic changes that occur during ARHI induction and their role in modulating death and dormancy are unknown. We employed Nuclear Magnetic Resonance (NMR)-based metabolomic strategies to characterize changes in key metabolic pathways in both cell culture and xenograft models of ARHI expression and autophagy. These pathways were further interrogated by cell-based immunofluorescence imaging, tracer uptake studies, targeted metabolic inhibition, and in vivo PET/CT imaging. Induction of ARHI in cell culture models resulted in an autophagy-dependent increase in lactate production along with increased glucose uptake and enhanced sensitivity to glycolytic inhibitors. Increased uptake of glutamine was also dependent on autophagy and dramatically sensitized cultured ARHI-expressing ovarian cancer cell lines to glutaminase inhibition. Induction of ARHI resulted in a reduction in mitochondrial respiration, decreased mitochondrial membrane potential, and decreased Tom20 staining suggesting an ARHI-dependent loss of mitochondrial function. ARHI induction in mouse xenograft models resulted in an increase in free amino acids, a transient increase in [18F]-FDG uptake, and significantly altered choline metabolism. ARHI expression has previously been shown to trigger autophagy-associated necroptosis in cell culture. In this study, we have demonstrated that ARHI expression results in decreased cellular ATP/ADP, increased oxidative stress, and decreased mitochondrial function. While this bioenergetic shock is consistent with programmed necrosis, our data indicates that the accompanying up-regulation of glycolysis and glutaminolysis is autophagy-dependent and serves to support cell viability rather than facilitate necroptotic cell death. While the mechanistic basis for metabolic up-regulation following ARHI induction is unknown, our preliminary data suggest that decreased mitochondrial function and increased metabolic demand may play a role. These alterations in fundamental metabolic pathways during autophagy-associated necroptosis may provide the basis for new therapeutic strategies for the treatment of dormant ovarian tumors.
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         Autophagy
         Metabolism
         Glutaminolysis
         Ovarian cancer
         NMR
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         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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      affiliation:
            name:the University of Texas M.D. Anderson Cancer Center
            address:
               name:Department of Experimental Therapeutics, the University of Texas M.D. Anderson Cancer Center, Houston, USA
               type:PostalAddress
            type:Organization
      name:Margie N. Sutton
      affiliation:
            name:the University of Texas M.D. Anderson Cancer Center
            address:
               name:Department of Experimental Therapeutics, the University of Texas M.D. Anderson Cancer Center, Houston, USA
               type:PostalAddress
            type:Organization
      name:Pratip K. Bhattacharya
      affiliation:
            name:the University of Texas M.D. Anderson Cancer Center
            address:
               name:Department of Cancer Systems Imaging, the University of Texas M.D. Anderson Cancer Center, Houston, USA
               type:PostalAddress
            type:Organization
      name:Robert C. Bast
      affiliation:
            name:the University of Texas M.D. Anderson Cancer Center
            address:
               name:Department of Experimental Therapeutics, the University of Texas M.D. Anderson Cancer Center, Houston, USA
               type:PostalAddress
            type:Organization
      name:Steven W. Millward
      affiliation:
            name:the University of Texas M.D. Anderson Cancer Center
            address:
               name:Department of Cancer Systems Imaging, the University of Texas M.D. Anderson Cancer Center, Houston, USA
               type:PostalAddress
            type:Organization
            name:Rice University
            address:
               name:Department of Bioengineering, Rice University, Houston, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Cancer Systems Imaging, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Cancer Systems Imaging, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Experimental Therapeutics, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Cancer Systems Imaging, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Bioengineering, Rice University, Houston, USA
      name:Department of Cancer Systems Imaging, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Cancer Systems Imaging, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Experimental Therapeutics, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Cancer Systems Imaging, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Experimental Therapeutics, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Experimental Therapeutics, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Experimental Therapeutics, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Cancer Systems Imaging, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Experimental Therapeutics, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Cancer Systems Imaging, the University of Texas M.D. Anderson Cancer Center, Houston, USA
      name:Department of Bioengineering, Rice University, Houston, USA

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