We are analyzing https://link.springer.com/article/10.1186/1471-2407-9-56.

Title:
Role of oxidative stress and intracellular glutathione in the sensitivity to apoptosis induced by proteasome inhibitor in thyroid cancer cells | BMC Cancer
Description:
Background The proteasome inhibitor bortezomib has shown impressive clinical activity alone and in combination with conventional and other novel agents for the treatment of multiple myeloma (MM) and some solid cancers. Although bortezomib is known to be a selective proteasome inhibitor, the downstream mechanisms of cytotoxicity and drug resistance are poorly understood. Methods Proteasome activity, intracellular glutathione (GSH) and ROS levels, as well as activities of GSH synthesis enzymes were measured using spectrophotometric methods. Cell death was analyzed using flow cytometry and caspase activity assay. The expression level of GSH synthesis enzymes were measured using real-time RT-PCR. Results At concentrations that effectively inhibited proteasome activity, bortezomib induced apoptosis in FRO cells, but not in ARO cells. Bortezomib elevated the amount of glutathione (GSH) and the treatment with bortezomib increased the level of mRNA for GCL, a rate-limiting enzyme in glutathione synthesis. Furthermore, depletion of GSH increases apoptosis induced by bortezomib, in contrast, repletion of GSH decreases bortezomib-mediated cell death. Conclusion GSH protects cells from proteasome inhibition-induced oxidative stress and glutathione-dependent redox system might play an important role in the sensitivity to proteasome inhibition-induced apoptosis.
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Keywords {🔍}

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Topics {✒️}

ac-asp-glu-val-asp-7-amino-4-methylcoumarin 5 mm l-γ-glutamyl-l-α-aminobutyrate yifu guan & hua-qin wang reactive oxygen species s-n-butyl homocysteine sulfoximine real-time rt-pcr pre-publication history redox-sensitive dye dcfh-da open access article copper/zinc-superoxide dismutase oxygen species hua-qin wang n-acetyl-l-cysteine real-time pcr real time pcr article download pdf related subjects multiple myeloma progressing fluorescence-activated cell scanner bortezomib-induced cell death proteasome inhibition-induced apoptosis arbitrary unit/mg protein mitogen-activated protein kinase glutathione-dependent redox system bortezomib-mediated ros release cell type-specific differences bortezomib-induced apoptotic death fluorophore 7-amino-4-methylcoumarin labeled substrate llvy-amc bortezomib-induced apoptotic signaling bortezomib-induced ros generation privacy choices/manage cookies cell death assays gsh monoethyl ester multiple myeloma authors’ original file fas-mediated apoptosis hai-yan zhang ebselen induces apoptosis anticancer drug resistance thyroid cancer cells induce cell death bortezomib-mediated apoptosis ac-devd-amc cell death signaling proteasome inhibitor ps-341 cancer drug resistance triggering cell death thyroid cancer treatment full access

Schema {🗺️}

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         description:The proteasome inhibitor bortezomib has shown impressive clinical activity alone and in combination with conventional and other novel agents for the treatment of multiple myeloma (MM) and some solid cancers. Although bortezomib is known to be a selective proteasome inhibitor, the downstream mechanisms of cytotoxicity and drug resistance are poorly understood. Proteasome activity, intracellular glutathione (GSH) and ROS levels, as well as activities of GSH synthesis enzymes were measured using spectrophotometric methods. Cell death was analyzed using flow cytometry and caspase activity assay. The expression level of GSH synthesis enzymes were measured using real-time RT-PCR. At concentrations that effectively inhibited proteasome activity, bortezomib induced apoptosis in FRO cells, but not in ARO cells. Bortezomib elevated the amount of glutathione (GSH) and the treatment with bortezomib increased the level of mRNA for GCL, a rate-limiting enzyme in glutathione synthesis. Furthermore, depletion of GSH increases apoptosis induced by bortezomib, in contrast, repletion of GSH decreases bortezomib-mediated cell death. GSH protects cells from proteasome inhibition-induced oxidative stress and glutathione-dependent redox system might play an important role in the sensitivity to proteasome inhibition-induced apoptosis.
         datePublished:2009-02-16T00:00:00Z
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      headline:Role of oxidative stress and intracellular glutathione in the sensitivity to apoptosis induced by proteasome inhibitor in thyroid cancer cells
      description:The proteasome inhibitor bortezomib has shown impressive clinical activity alone and in combination with conventional and other novel agents for the treatment of multiple myeloma (MM) and some solid cancers. Although bortezomib is known to be a selective proteasome inhibitor, the downstream mechanisms of cytotoxicity and drug resistance are poorly understood. Proteasome activity, intracellular glutathione (GSH) and ROS levels, as well as activities of GSH synthesis enzymes were measured using spectrophotometric methods. Cell death was analyzed using flow cytometry and caspase activity assay. The expression level of GSH synthesis enzymes were measured using real-time RT-PCR. At concentrations that effectively inhibited proteasome activity, bortezomib induced apoptosis in FRO cells, but not in ARO cells. Bortezomib elevated the amount of glutathione (GSH) and the treatment with bortezomib increased the level of mRNA for GCL, a rate-limiting enzyme in glutathione synthesis. Furthermore, depletion of GSH increases apoptosis induced by bortezomib, in contrast, repletion of GSH decreases bortezomib-mediated cell death. GSH protects cells from proteasome inhibition-induced oxidative stress and glutathione-dependent redox system might play an important role in the sensitivity to proteasome inhibition-induced apoptosis.
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         Bortezomib
         Reactive Oxygen Species Generation
         GSSG
         Reactive Oxygen Species Level
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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               type:PostalAddress
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            name:China Medical University
            address:
               name:Department of Geriatrics, the 1st Affiliated Hospital, China Medical University, Shenyang, P.R. China
               type:PostalAddress
            type:Organization
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      affiliation:
            name:China Medical University
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               type:PostalAddress
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      name:Department of Biochemistry and Molecular Biology, China Medical University, Shenyang, P.R. China
      name:Department of Biochemistry and Molecular Biology, China Medical University, Shenyang, P.R. China
      name:Department of Biochemistry and Molecular Biology, China Medical University, Shenyang, P.R. China

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