Oncometabolic role of mitochondrial sirtuins in glioma patients
Mitochondrial sirtuins have diverse role specifically in aging, metabolism and cancer. In cancer, these sirtuins play dichotomous role as tumor suppressor and promoter. Previous studies have reported the involvement of sirtuins in different cancers. However, till now no study has been published with...
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| description | Mitochondrial sirtuins have diverse role specifically in aging, metabolism and cancer. In cancer, these sirtuins play dichotomous role as tumor suppressor and promoter. Previous studies have reported the involvement of sirtuins in different cancers. However, till now no study has been published with respect to mitochondrial sirtuins and glioma risks. Present study was purposed to figure out the expression level of mitochondrial sirtuins (SIRT3, SIRT4, SIRT5) and related genes (GDH, OGG1-2α, SOD1, SOD2, HIF1α and PARP1) in 153 glioma tissue samples and 200 brain tissue samples from epilepsy patients (taken as controls). To understand the role of selected situins in gliomagenesis, DNA damage was measured using the comet assay and oncometabolic role (oxidative stress level, ATP level and NAD level) was measured using the ELISA and quantitative PCR. Results analysis showed significant down-regulation of SIRT4 (p = 0.0337), SIRT5 (p |
| doi_str_mv | 10.1371/journal.pone.0281840 |
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In cancer, these sirtuins play dichotomous role as tumor suppressor and promoter. Previous studies have reported the involvement of sirtuins in different cancers. However, till now no study has been published with respect to mitochondrial sirtuins and glioma risks. Present study was purposed to figure out the expression level of mitochondrial sirtuins (SIRT3, SIRT4, SIRT5) and related genes (GDH, OGG1-2α, SOD1, SOD2, HIF1α and PARP1) in 153 glioma tissue samples and 200 brain tissue samples from epilepsy patients (taken as controls). To understand the role of selected situins in gliomagenesis, DNA damage was measured using the comet assay and oncometabolic role (oxidative stress level, ATP level and NAD level) was measured using the ELISA and quantitative PCR. Results analysis showed significant down-regulation of SIRT4 (p = 0.0337), SIRT5 (p<0.0001), GDH (p = 0.0305), OGG1-2α (p = 0.0001), SOD1 (p<0.0001) and SOD2 (p<0.0001) in glioma patients compared to controls. In case of SIRT3 (p = 0.0322), HIF1α (p = 0.0385) and PARP1 (p = 0.0203), significant up-regulation was observed. ROC curve analysis and cox regression analysis showed the good diagnostic and prognostic value of mitochondrial sirtuins in glioma patients. Oncometabolic rate assessment analysis showed significant increased ATP level (p<0.0001), NAD+ level [(NMNAT1 (p<0.0001), NMNAT3 (p<0.0001) and NAMPT (p<0.04)] and glutathione level (p<0.0001) in glioma patients compared to controls. Significant increased level of damage ((p<0.04) and decrease level of antioxidant enzymes include superoxide dismutase (SOD, p<0.0001), catalase (CAT, p<0.0001) and glutathione peroxidase (GPx, p<0.0001) was observed in patients compared to controls. Present study data suggest that variation in expression pattern of mitochondrial sirtuins and increased metabolic rate may have diagnostic and prognostic significance in glioma patients.]]></description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0281840</identifier><identifier>PMID: 36809279</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adenosine Triphosphate ; Analysis ; Apoptosis ; ATP ; Bioassays ; Biology and Life Sciences ; Brain cancer ; Brain tumors ; Breast cancer ; Cancer ; Catalase ; Cell cycle ; Colorectal cancer ; Comet assay ; Damage detection ; Datasets ; Deoxyribonucleic acid ; Diagnostic systems ; DNA ; DNA damage ; Enzyme-linked immunosorbent assay ; Enzymes ; Epilepsy ; Gastric cancer ; Gene expression ; Genes ; Genetic aspects ; Genetic markers ; Genomes ; Glioma ; Gliomas ; Glutathione ; Glutathione peroxidase ; Health aspects ; Humans ; Medicine and Health Sciences ; Metabolic rate ; Metabolism ; Mitochondria ; Mitochondrial DNA ; Mitochondrial Proteins - metabolism ; Mutation ; Nicotinamide-Nucleotide Adenylyltransferase - metabolism ; OGG1 protein ; Oncology, Experimental ; Oxidative stress ; Peroxidase ; Poly(ADP-ribose) polymerase ; Prevention ; Proteins ; Regression analysis ; Risk factors ; Sirtuin 3 - genetics ; Sirtuins ; Sirtuins - metabolism ; Stress measurement ; Superoxide ; Superoxide dismutase ; Superoxide Dismutase-1 - metabolism ; Thyroid cancer ; Toxicity ; Tumor suppressor genes ; Tumors</subject><ispartof>PloS one, 2023-02, Vol.18 (2), p.e0281840-e0281840</ispartof><rights>Copyright: © 2023 Haq et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</rights><rights>COPYRIGHT 2023 Public Library of Science</rights><rights>2023 Haq et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 Haq et al 2023 Haq et al</rights><rights>2023 Haq et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-c8215d960ce3b799f2c64adfcbe335becb6cc67429fb2b0154f24c7b36c377433</citedby><cites>FETCH-LOGICAL-c692t-c8215d960ce3b799f2c64adfcbe335becb6cc67429fb2b0154f24c7b36c377433</cites><orcidid>0000-0001-9886-180X ; 0000-0002-6392-672X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9943017/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9943017/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36809279$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Di Zazzo, Erika</contributor><creatorcontrib>Haq, Maria Fazal Ul</creatorcontrib><creatorcontrib>Hussain, Muhammad Zahid</creatorcontrib><creatorcontrib>Mahjabeen, Ishrat</creatorcontrib><creatorcontrib>Akram, Zertashia</creatorcontrib><creatorcontrib>Saeed, Nadia</creatorcontrib><creatorcontrib>Shafique, Rabia</creatorcontrib><creatorcontrib>Abbasi, Sumaira Fida</creatorcontrib><creatorcontrib>Kayani, Mahmood Akhtar</creatorcontrib><title>Oncometabolic role of mitochondrial sirtuins in glioma patients</title><title>PloS one</title><addtitle>PLoS One</addtitle><description><![CDATA[Mitochondrial sirtuins have diverse role specifically in aging, metabolism and cancer. In cancer, these sirtuins play dichotomous role as tumor suppressor and promoter. Previous studies have reported the involvement of sirtuins in different cancers. However, till now no study has been published with respect to mitochondrial sirtuins and glioma risks. Present study was purposed to figure out the expression level of mitochondrial sirtuins (SIRT3, SIRT4, SIRT5) and related genes (GDH, OGG1-2α, SOD1, SOD2, HIF1α and PARP1) in 153 glioma tissue samples and 200 brain tissue samples from epilepsy patients (taken as controls). To understand the role of selected situins in gliomagenesis, DNA damage was measured using the comet assay and oncometabolic role (oxidative stress level, ATP level and NAD level) was measured using the ELISA and quantitative PCR. Results analysis showed significant down-regulation of SIRT4 (p = 0.0337), SIRT5 (p<0.0001), GDH (p = 0.0305), OGG1-2α (p = 0.0001), SOD1 (p<0.0001) and SOD2 (p<0.0001) in glioma patients compared to controls. In case of SIRT3 (p = 0.0322), HIF1α (p = 0.0385) and PARP1 (p = 0.0203), significant up-regulation was observed. ROC curve analysis and cox regression analysis showed the good diagnostic and prognostic value of mitochondrial sirtuins in glioma patients. Oncometabolic rate assessment analysis showed significant increased ATP level (p<0.0001), NAD+ level [(NMNAT1 (p<0.0001), NMNAT3 (p<0.0001) and NAMPT (p<0.04)] and glutathione level (p<0.0001) in glioma patients compared to controls. Significant increased level of damage ((p<0.04) and decrease level of antioxidant enzymes include superoxide dismutase (SOD, p<0.0001), catalase (CAT, p<0.0001) and glutathione peroxidase (GPx, p<0.0001) was observed in patients compared to controls. Present study data suggest that variation in expression pattern of mitochondrial sirtuins and increased metabolic rate may have diagnostic and prognostic significance in glioma patients.]]></description><subject>Adenosine Triphosphate</subject><subject>Analysis</subject><subject>Apoptosis</subject><subject>ATP</subject><subject>Bioassays</subject><subject>Biology and Life Sciences</subject><subject>Brain cancer</subject><subject>Brain tumors</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Catalase</subject><subject>Cell cycle</subject><subject>Colorectal cancer</subject><subject>Comet assay</subject><subject>Damage detection</subject><subject>Datasets</subject><subject>Deoxyribonucleic acid</subject><subject>Diagnostic systems</subject><subject>DNA</subject><subject>DNA damage</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Enzymes</subject><subject>Epilepsy</subject><subject>Gastric cancer</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic markers</subject><subject>Genomes</subject><subject>Glioma</subject><subject>Gliomas</subject><subject>Glutathione</subject><subject>Glutathione peroxidase</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Medicine and Health Sciences</subject><subject>Metabolic rate</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Mitochondrial DNA</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>Mutation</subject><subject>Nicotinamide-Nucleotide Adenylyltransferase - metabolism</subject><subject>OGG1 protein</subject><subject>Oncology, Experimental</subject><subject>Oxidative stress</subject><subject>Peroxidase</subject><subject>Poly(ADP-ribose) polymerase</subject><subject>Prevention</subject><subject>Proteins</subject><subject>Regression analysis</subject><subject>Risk factors</subject><subject>Sirtuin 3 - genetics</subject><subject>Sirtuins</subject><subject>Sirtuins - metabolism</subject><subject>Stress measurement</subject><subject>Superoxide</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase-1 - metabolism</subject><subject>Thyroid cancer</subject><subject>Toxicity</subject><subject>Tumor suppressor 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Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Haq, Maria Fazal Ul</au><au>Hussain, Muhammad Zahid</au><au>Mahjabeen, Ishrat</au><au>Akram, Zertashia</au><au>Saeed, Nadia</au><au>Shafique, Rabia</au><au>Abbasi, Sumaira Fida</au><au>Kayani, Mahmood Akhtar</au><au>Di Zazzo, Erika</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oncometabolic role of mitochondrial sirtuins in glioma patients</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2023-02-21</date><risdate>2023</risdate><volume>18</volume><issue>2</issue><spage>e0281840</spage><epage>e0281840</epage><pages>e0281840-e0281840</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract><![CDATA[Mitochondrial sirtuins have diverse role specifically in aging, metabolism and cancer. In cancer, these sirtuins play dichotomous role as tumor suppressor and promoter. Previous studies have reported the involvement of sirtuins in different cancers. However, till now no study has been published with respect to mitochondrial sirtuins and glioma risks. Present study was purposed to figure out the expression level of mitochondrial sirtuins (SIRT3, SIRT4, SIRT5) and related genes (GDH, OGG1-2α, SOD1, SOD2, HIF1α and PARP1) in 153 glioma tissue samples and 200 brain tissue samples from epilepsy patients (taken as controls). To understand the role of selected situins in gliomagenesis, DNA damage was measured using the comet assay and oncometabolic role (oxidative stress level, ATP level and NAD level) was measured using the ELISA and quantitative PCR. Results analysis showed significant down-regulation of SIRT4 (p = 0.0337), SIRT5 (p<0.0001), GDH (p = 0.0305), OGG1-2α (p = 0.0001), SOD1 (p<0.0001) and SOD2 (p<0.0001) in glioma patients compared to controls. In case of SIRT3 (p = 0.0322), HIF1α (p = 0.0385) and PARP1 (p = 0.0203), significant up-regulation was observed. ROC curve analysis and cox regression analysis showed the good diagnostic and prognostic value of mitochondrial sirtuins in glioma patients. Oncometabolic rate assessment analysis showed significant increased ATP level (p<0.0001), NAD+ level [(NMNAT1 (p<0.0001), NMNAT3 (p<0.0001) and NAMPT (p<0.04)] and glutathione level (p<0.0001) in glioma patients compared to controls. Significant increased level of damage ((p<0.04) and decrease level of antioxidant enzymes include superoxide dismutase (SOD, p<0.0001), catalase (CAT, p<0.0001) and glutathione peroxidase (GPx, p<0.0001) was observed in patients compared to controls. Present study data suggest that variation in expression pattern of mitochondrial sirtuins and increased metabolic rate may have diagnostic and prognostic significance in glioma patients.]]></abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>36809279</pmid><doi>10.1371/journal.pone.0281840</doi><tpages>e0281840</tpages><orcidid>https://orcid.org/0000-0001-9886-180X</orcidid><orcidid>https://orcid.org/0000-0002-6392-672X</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2023-02, Vol.18 (2), p.e0281840-e0281840 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2778594877 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Adenosine Triphosphate Analysis Apoptosis ATP Bioassays Biology and Life Sciences Brain cancer Brain tumors Breast cancer Cancer Catalase Cell cycle Colorectal cancer Comet assay Damage detection Datasets Deoxyribonucleic acid Diagnostic systems DNA DNA damage Enzyme-linked immunosorbent assay Enzymes Epilepsy Gastric cancer Gene expression Genes Genetic aspects Genetic markers Genomes Glioma Gliomas Glutathione Glutathione peroxidase Health aspects Humans Medicine and Health Sciences Metabolic rate Metabolism Mitochondria Mitochondrial DNA Mitochondrial Proteins - metabolism Mutation Nicotinamide-Nucleotide Adenylyltransferase - metabolism OGG1 protein Oncology, Experimental Oxidative stress Peroxidase Poly(ADP-ribose) polymerase Prevention Proteins Regression analysis Risk factors Sirtuin 3 - genetics Sirtuins Sirtuins - metabolism Stress measurement Superoxide Superoxide dismutase Superoxide Dismutase-1 - metabolism Thyroid cancer Toxicity Tumor suppressor genes Tumors |
| title | Oncometabolic role of mitochondrial sirtuins in glioma patients |
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