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Topics {✒️}

small-molecule bcl-2/bcl-xl inhibitor tumor suppressors mir-125a-5p inhibitory cue-reward associations sensory cortical plasticity multi-step collagenase procedure dual-mode imaging system acetaminophen-induced cell death mouse paraffin-embedded sections tumor suppressors mir-125a suppressing p53-dependent cytotoxicity human hepatocellular carcinoma dna damage p53-dependent apoptosis pathway tace-resistant hcc showed regulating doxorubicin-induced apoptosis unresectable hepatocellular carcinoma p53-dependent apoptosis machinery mitogen-activated protein kinase sirt7-dependent acetylation switch foxo1-pdx1-glut2 pathway epigenetically inhibiting mir-34a p53-dependent noxa expression p53-binding consensus sequence cfx96 real-time system histone deacetylase inhibition doxorubicin-induced mapk activation kaplan–meier analysis revealed significantly increased intensity article download pdf wild type flag-p53 investigate sirt7-dependent deacetylation stain nuclear dna sirt7-dependent p53 regulation serine-574 phosphorylation regulates liver cancer tissues p53-double kr mutants p53 overexpression-enhanced portion mitochondrial death machinery hepatocellular carcinomas identifies squamous cell carcinoma cancer drug resistance p53-null hep3b cells sirt7 completely abolished full access underlying hcc response zhuan li hepatocellular carcinoma mitochondrial apoptotic pathway acetyl-transferase p300 increased cell death

Questions {❓}

• Targeting the mitochondrial apoptotic pathway: a preferred approach in hematologic malignancies?

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         headline:SIRT7 regulates hepatocellular carcinoma response to therapy by altering the p53-dependent cell death pathway
         description:Optimal therapeutic strategies for hepatocellular carcinoma (HCC) patients are still challenging due to the high recurrence rate after surgical resection and chemotherapy resistance. Growing evidence shows that genetic and epigenetic alterations are involved in HCC progression and resistance to therapy, however the molecular mechanisms underlying resistance to therapy have not been fully understood. Expression of SIRT7 in 17 paired paraffin-embedded HCC tissues and adjacent nontumoral liver tissues was examined by immunohistochemistry and Western blot. The mRNA expression of SIRT7 in 20 paired frozen HCC tissues and adjacent nontumoral liver tissues was analyzed by quantitative RT-PCR. The biologic consequences of overexpression and knockdown of SIRT7 in HCC therapy sensitivity were studied in vitro and in vivo. Interaction between SIRT7 and p53 were studied in HCC cell lines. SIRT7 expression was frequently upregulated in clinical HCC samples, and its expression was highly associated with TACE-resistance and poor survival (P = 0.008.) Depletion of SIRT7 from multiple liver cancer cell lines significantly increased doxorubicin toxicity while overexpression of SIRT7 largely abolished doxorubicin induced apoptosis. At the molecular level, we observed that SIRT7 interacts with and induces deacetylation of p53 at lysines 320 and 373. Deacetylated p53 showed significantly less affinity for the NOXA promoter and its transcription. In mouse xenografts, SIRT7 suppression increased doxorubicin induced p53 activation, inhibited tumor growth and induced apoptosis. The newly identified SIRT7-p53-NOXA axis partially illustrates the molecular mechanism of HCC resistance to therapy and represents a novel potential therapeutic target for HCC treatment.
         datePublished:2019-06-13T00:00:00Z
         dateModified:2019-06-13T00:00:00Z
         pageStart:1
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         license:http://creativecommons.org/publicdomain/zero/1.0/
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            Histone deacetylase
            HCC
            TACE resistance
            NOXA
            Deacetylation
            Cancer Research
            Immunology
            Apoptosis
            Oncology
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      headline:SIRT7 regulates hepatocellular carcinoma response to therapy by altering the p53-dependent cell death pathway
      description:Optimal therapeutic strategies for hepatocellular carcinoma (HCC) patients are still challenging due to the high recurrence rate after surgical resection and chemotherapy resistance. Growing evidence shows that genetic and epigenetic alterations are involved in HCC progression and resistance to therapy, however the molecular mechanisms underlying resistance to therapy have not been fully understood. Expression of SIRT7 in 17 paired paraffin-embedded HCC tissues and adjacent nontumoral liver tissues was examined by immunohistochemistry and Western blot. The mRNA expression of SIRT7 in 20 paired frozen HCC tissues and adjacent nontumoral liver tissues was analyzed by quantitative RT-PCR. The biologic consequences of overexpression and knockdown of SIRT7 in HCC therapy sensitivity were studied in vitro and in vivo. Interaction between SIRT7 and p53 were studied in HCC cell lines. SIRT7 expression was frequently upregulated in clinical HCC samples, and its expression was highly associated with TACE-resistance and poor survival (P = 0.008.) Depletion of SIRT7 from multiple liver cancer cell lines significantly increased doxorubicin toxicity while overexpression of SIRT7 largely abolished doxorubicin induced apoptosis. At the molecular level, we observed that SIRT7 interacts with and induces deacetylation of p53 at lysines 320 and 373. Deacetylated p53 showed significantly less affinity for the NOXA promoter and its transcription. In mouse xenografts, SIRT7 suppression increased doxorubicin induced p53 activation, inhibited tumor growth and induced apoptosis. The newly identified SIRT7-p53-NOXA axis partially illustrates the molecular mechanism of HCC resistance to therapy and represents a novel potential therapeutic target for HCC treatment.
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      dateModified:2019-06-13T00:00:00Z
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      keywords:
         Histone deacetylase
         HCC
         TACE resistance
         NOXA
         Deacetylation
         Cancer Research
         Immunology
         Apoptosis
         Oncology
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      name:Department of Internal Medicine, University of Kansas Medical Center, Kansas City, USA
      name:Department of Internal Medicine, University of Kansas Medical Center, Kansas City, USA
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      name:Department of Internal Medicine, University of Kansas Medical Center, Kansas City, USA
      name:Liver Center, University of Kansas Medical Center, Kansas City, USA
      name:Department of Internal Medicine, University of Kansas Medical Center, Kansas City, USA

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