We are analyzing https://link.springer.com/article/10.1186/s12967-022-03447-y.

Title:
Platinum-induced mitochondrial OXPHOS contributes to cancer stem cell enrichment in ovarian cancer | Journal of Translational Medicine
Description:
Background Platinum based agents—cisplatin and carboplatin in combination with taxanes are used for the treatment of ovarian cancer (OC) patients. However, the majority of OC patients develop recurrent, platinum resistant disease that is uniformly fatal. Platinum treatment enriches for chemoresistant aldehyde dehydrogenase (ALDH) + ovarian cancer stem cells (OCSCs), which contribute to tumor recurrence and disease relapse. Acquired platinum resistance also includes metabolic reprograming and switching to oxidative phosphorylation (OXPHOS). Chemosensitive cells rely on glycolysis while chemoresistant cells have the ability to switch between glycolysis and OXPHOS, depending on which pathway drives a selective advantage for growth and chemoresistance. High expression of genes involved in OXPHOS and high production of mitochondrial ROS are characteristics of OCSCs, suggesting that OCSCs favor OXPHOS over glycolysis. Based on connections between OCSCs, chemoresistance and OXPHOS, we hypothesize that platinum treatment induces changes in metabolism that contribute to platinum-induced enrichment of OCSCs. Methods The effect of cisplatin on mitochondrial activity was assessed by JC1 staining and expression of OXPHOS genes by RT-qPCR. Cisplatin-induced changes in Sirtuin 1 (SIRT1) levels and activity were assessed by western blot. Small molecule inhibitors of mitochondrial complex I and SIRT1 were used to determine if their enzymatic activity contributes to the platinum-induced enrichment of OCSCs. The percentage of ALDH + OCSCs in OC cells and tumor tissue from xenograft models across different treatment conditions was analyzed using ALDEFLUOR assay and flow cytometry. Results We demonstrate that platinum treatment increases mitochondrial activity. Combined treatment of platinum agents and OXPHOS inhibitors blocks the platinum-induced enrichment of ALDH + OCSCs in vitro and in vivo. Furthermore, platinum treatment increases SIRT1 levels and subsequent deacetylase activity, which likely contributes to the increase in platinum-induced mitochondrial activity. Conclusions These findings on metabolic pathways altered by platinum-based chemotherapy have uncovered key targets that can be exploited therapeutically to block the platinum-induced enrichment of OCSCs, ultimately improving the survival of OC patients.
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Keywords {🔍}

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Topics {✒️}

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Questions {❓}

AMPK and SIRT1: a long-standing partnership?
Cancer stem cells: mirage or reality?
Ovarian cancer stem cells: still an elusive entity?
Targeting sirtuin 1 to improve metabolism: all you need is NAD(+)?

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         headline:Platinum-induced mitochondrial OXPHOS contributes to cancer stem cell enrichment in ovarian cancer
         description:Platinum based agents—cisplatin and carboplatin in combination with taxanes are used for the treatment of ovarian cancer (OC) patients. However, the majority of OC patients develop recurrent, platinum resistant disease that is uniformly fatal. Platinum treatment enriches for chemoresistant aldehyde dehydrogenase (ALDH) + ovarian cancer stem cells (OCSCs), which contribute to tumor recurrence and disease relapse. Acquired platinum resistance also includes metabolic reprograming and switching to oxidative phosphorylation (OXPHOS). Chemosensitive cells rely on glycolysis while chemoresistant cells have the ability to switch between glycolysis and OXPHOS, depending on which pathway drives a selective advantage for growth and chemoresistance. High expression of genes involved in OXPHOS and high production of mitochondrial ROS are characteristics of OCSCs, suggesting that OCSCs favor OXPHOS over glycolysis. Based on connections between OCSCs, chemoresistance and OXPHOS, we hypothesize that platinum treatment induces changes in metabolism that contribute to platinum-induced enrichment of OCSCs. The effect of cisplatin on mitochondrial activity was assessed by JC1 staining and expression of OXPHOS genes by RT-qPCR. Cisplatin-induced changes in Sirtuin 1 (SIRT1) levels and activity were assessed by western blot. Small molecule inhibitors of mitochondrial complex I and SIRT1 were used to determine if their enzymatic activity contributes to the platinum-induced enrichment of OCSCs. The percentage of ALDH + OCSCs in OC cells and tumor tissue from xenograft models across different treatment conditions was analyzed using ALDEFLUOR assay and flow cytometry. We demonstrate that platinum treatment increases mitochondrial activity. Combined treatment of platinum agents and OXPHOS inhibitors blocks the platinum-induced enrichment of ALDH + OCSCs in vitro and in vivo. Furthermore, platinum treatment increases SIRT1 levels and subsequent deacetylase activity, which likely contributes to the increase in platinum-induced mitochondrial activity. These findings on metabolic pathways altered by platinum-based chemotherapy have uncovered key targets that can be exploited therapeutically to block the platinum-induced enrichment of OCSCs, ultimately improving the survival of OC patients.
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      headline:Platinum-induced mitochondrial OXPHOS contributes to cancer stem cell enrichment in ovarian cancer
      description:Platinum based agents—cisplatin and carboplatin in combination with taxanes are used for the treatment of ovarian cancer (OC) patients. However, the majority of OC patients develop recurrent, platinum resistant disease that is uniformly fatal. Platinum treatment enriches for chemoresistant aldehyde dehydrogenase (ALDH) + ovarian cancer stem cells (OCSCs), which contribute to tumor recurrence and disease relapse. Acquired platinum resistance also includes metabolic reprograming and switching to oxidative phosphorylation (OXPHOS). Chemosensitive cells rely on glycolysis while chemoresistant cells have the ability to switch between glycolysis and OXPHOS, depending on which pathway drives a selective advantage for growth and chemoresistance. High expression of genes involved in OXPHOS and high production of mitochondrial ROS are characteristics of OCSCs, suggesting that OCSCs favor OXPHOS over glycolysis. Based on connections between OCSCs, chemoresistance and OXPHOS, we hypothesize that platinum treatment induces changes in metabolism that contribute to platinum-induced enrichment of OCSCs. The effect of cisplatin on mitochondrial activity was assessed by JC1 staining and expression of OXPHOS genes by RT-qPCR. Cisplatin-induced changes in Sirtuin 1 (SIRT1) levels and activity were assessed by western blot. Small molecule inhibitors of mitochondrial complex I and SIRT1 were used to determine if their enzymatic activity contributes to the platinum-induced enrichment of OCSCs. The percentage of ALDH + OCSCs in OC cells and tumor tissue from xenograft models across different treatment conditions was analyzed using ALDEFLUOR assay and flow cytometry. We demonstrate that platinum treatment increases mitochondrial activity. Combined treatment of platinum agents and OXPHOS inhibitors blocks the platinum-induced enrichment of ALDH + OCSCs in vitro and in vivo. Furthermore, platinum treatment increases SIRT1 levels and subsequent deacetylase activity, which likely contributes to the increase in platinum-induced mitochondrial activity. These findings on metabolic pathways altered by platinum-based chemotherapy have uncovered key targets that can be exploited therapeutically to block the platinum-induced enrichment of OCSCs, ultimately improving the survival of OC patients.
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         Chemoresistance
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         SIRT1
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         general
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               name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
               type:PostalAddress
            type:Organization
      name:Tara X. Metcalfe
      affiliation:
            name:Indiana University School of Medicine
            address:
               name:Cell, Molecular and Cancer Biology Graduate Program, Indiana University School of Medicine, Bloomington, USA
               type:PostalAddress
            type:Organization
            name:Indiana University School of Medicine
            address:
               name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
               type:PostalAddress
            type:Organization
      name:Weini Wang
      affiliation:
            name:Indiana University School of Medicine
            address:
               name:Cell, Molecular and Cancer Biology Graduate Program, Indiana University School of Medicine, Bloomington, USA
               type:PostalAddress
            type:Organization
            name:Indiana University School of Medicine
            address:
               name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
               type:PostalAddress
            type:Organization
      name:Kenneth P. Nephew
      affiliation:
            name:Indiana University School of Medicine
            address:
               name:Cell, Molecular and Cancer Biology Graduate Program, Indiana University School of Medicine, Bloomington, USA
               type:PostalAddress
            type:Organization
            name:Indiana University School of Medicine
            address:
               name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
               type:PostalAddress
            type:Organization
            name:Indiana University Bloomington
            address:
               name:Genome, Cell and Developmental Biology, Department of Biology, Indiana University Bloomington, Bloomington, USA
               type:PostalAddress
            type:Organization
            name:Indiana University Melvin and Bren Simon Comprehensive Cancer Center
            address:
               name:Indiana University Melvin and Bren Simon Comprehensive Cancer Center, Indianapolis, USA
               type:PostalAddress
            type:Organization
            name:Indiana University School of Medicine
            address:
               name:Department of Anatomy, Cell Biology and Physiology, Department of Obstetrics and Gynecology, Indiana University School of Medicine, Indianapolis, USA
               type:PostalAddress
            type:Organization
      name:Heather M. O’Hagan
      url:http://orcid.org/0000-0001-9750-5088
      affiliation:
            name:Indiana University School of Medicine
            address:
               name:Cell, Molecular and Cancer Biology Graduate Program, Indiana University School of Medicine, Bloomington, USA
               type:PostalAddress
            type:Organization
            name:Indiana University School of Medicine
            address:
               name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
               type:PostalAddress
            type:Organization
            name:Indiana University Bloomington
            address:
               name:Genome, Cell and Developmental Biology, Department of Biology, Indiana University Bloomington, Bloomington, USA
               type:PostalAddress
            type:Organization
            name:Indiana University Melvin and Bren Simon Comprehensive Cancer Center
            address:
               name:Indiana University Melvin and Bren Simon Comprehensive Cancer Center, Indianapolis, USA
               type:PostalAddress
            type:Organization
            name:Indiana University School of Medicine
            address:
               name:Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, USA
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      email:[email protected]
PostalAddress:
      name:Cell, Molecular and Cancer Biology Graduate Program, Indiana University School of Medicine, Bloomington, USA
      name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
      name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
      name:Genome, Cell and Developmental Biology, Department of Biology, Indiana University Bloomington, Bloomington, USA
      name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
      name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
      name:Genome, Cell and Developmental Biology, Department of Biology, Indiana University Bloomington, Bloomington, USA
      name:Cell, Molecular and Cancer Biology Graduate Program, Indiana University School of Medicine, Bloomington, USA
      name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
      name:Cell, Molecular and Cancer Biology Graduate Program, Indiana University School of Medicine, Bloomington, USA
      name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
      name:Cell, Molecular and Cancer Biology Graduate Program, Indiana University School of Medicine, Bloomington, USA
      name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
      name:Cell, Molecular and Cancer Biology Graduate Program, Indiana University School of Medicine, Bloomington, USA
      name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
      name:Genome, Cell and Developmental Biology, Department of Biology, Indiana University Bloomington, Bloomington, USA
      name:Indiana University Melvin and Bren Simon Comprehensive Cancer Center, Indianapolis, USA
      name:Department of Anatomy, Cell Biology and Physiology, Department of Obstetrics and Gynecology, Indiana University School of Medicine, Indianapolis, USA
      name:Cell, Molecular and Cancer Biology Graduate Program, Indiana University School of Medicine, Bloomington, USA
      name:Medical Sciences Program, Indiana University School of Medicine, Bloomington, USA
      name:Genome, Cell and Developmental Biology, Department of Biology, Indiana University Bloomington, Bloomington, USA
      name:Indiana University Melvin and Bren Simon Comprehensive Cancer Center, Indianapolis, USA
      name:Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, USA

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