Insulin and IGF-1 extend the lifespan of Caenorhabditis elegans by inhibiting insulin/insulin-like signaling and mTOR signaling pathways: C. elegans - Focused cancer research

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dc.contributor.authorBerk, Seyda
dc.date.accessioned2024-10-26T18:02:33Z
dc.date.available2024-10-26T18:02:33Z
dc.date.issued2024
dc.departmentSivas Cumhuriyet Üniversitesi
dc.description.abstractThe mutations in Caenorhabditis elegans (C. elegans) that extend lifespan slow down aging by interfering with several signaling pathways, including the insulin/IGF-1 signaling (IIS) pathway, AMP-activated protein kinase (AMPK), and mechanistic target of rapamycin (mTOR). The tumor suppressor pRb (retinoblastoma protein) is believed to be involved in almost all human cancers. Lin-35, the C. elegans orthologue of the tumor suppressor pRb, was included in the study to explore the effects of insulin and IGF-1 because it has been linked to cancerrelated pRb function in mammals and exhibits a tumor suppressor effect by inhibiting mTOR or IIS signaling. According to our results, IGF-1 or insulin increased the lifespan of lin-35 worms compared to N2 worms by increasing fertilization efficiency, also causing a significant increase in body size. It was concluded that the expression of daf-2 and rsks-1 decreased after insulin or IGF-1 administration, thus extending the lifespan of C. elegans lin-35 worms through both IIS and mTOR-dependent mechanisms. This suggests that it was mediated by the combined effect of the TOR and IIS pathways. These results, especially obtained in cancer-associated mutant lin-35 worms, will be useful in elucidating the C. elegans cancer model in the future.
dc.description.sponsorshipAdvanced Technology and Research Center (CUTAM) , Sivas Cumhuriyet Univer-sity
dc.description.sponsorshipProject support was provided by Sivas Cumhuriyet University Scientific Research Projects (CUBAP) (Grant No. F-2021-651) , Turkiye.r The authors are thankful for the ongoing support of the Advanced Technology and Research Center (CUTAM) , Sivas Cumhuriyet Univer-sity, Turkiye. Further, we would like to thank Ozgur zgur Ulku Ozdemir, zdemir, master student of the Department of Molecular Biology and Genetics at Sivas Cumhuriyet University, Turkiye, for providing the necessary convenience and encouragement for the maintain of the C. elegans culture.
dc.identifier.doi10.1016/j.bbrc.2024.150347
dc.identifier.issn0006-291X
dc.identifier.issn1090-2104
dc.identifier.pmid38976945
dc.identifier.scopus2-s2.0-85197644364
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.1016/j.bbrc.2024.150347
dc.identifier.urihttps://hdl.handle.net/20.500.12418/28214
dc.identifier.volume729
dc.identifier.wosWOS:001266859800001
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherAcademic Press Inc Elsevier Science
dc.relation.ispartofBiochemical and Biophysical Research Communications
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectAgeing
dc.subjectC. elegans
dc.subjectInsulin
dc.subjectIGF-1
dc.subjectIGF-System
dc.subjectLifespan
dc.subjectLin-35
dc.subjectmTOR
dc.titleInsulin and IGF-1 extend the lifespan of Caenorhabditis elegans by inhibiting insulin/insulin-like signaling and mTOR signaling pathways: C. elegans - Focused cancer research
dc.typeArticle

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