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         headline:RETRACTED ARTICLE: Melatonin attenuates the TLR4-mediated inflammatory response through MyD88- and TRIF-dependent signaling pathways in an in vivo model of ovarian cancer
         description:Toll-like receptors (TLRs) are effector molecules expressed on the surface of ovarian cancer (OC) cells, but the functions of the TLR2/TLR4 signaling pathways in these cells remain unclear. Melatonin (mel) acts as an anti-inflammatory factor and has been reported to modulate TLRs in some aggressive tumor cell types. Therefore, we investigated OC and the effect of long-term mel therapy on the signaling pathways mediated by TLR2 and TLR4 via myeloid differentiation factor 88 (MyD88) and toll-like receptor-associated activator of interferon (TRIF) in an ethanol-preferring rat model. To induce OC, the left ovary of animals either consuming 10% (v/v) ethanol or not was injected directly under the bursa with a single dose of 100 μg of 7,12-dimethylbenz(a)anthracene (DMBA) dissolved in 10 μL of sesame oil. The right ovaries were used as sham-surgery controls. After developing OC, half of the animals received i.p. injections of mel (200 μg/100 g b.w./day) for 60 days. Although mel therapy was unable to reduce TLR2 levels, it was able to suppress the OC-associated increase in the levels of the following proteins: TLR4, MyD88, nuclear factor kappa B (NFkB p65), inhibitor of NFkB alpha (IkBα), IkB kinase alpha (IKK-α), TNF receptor-associated factor 6 (TRAF6), TRIF, interferon regulatory factor 3 (IRF3), interferon β (IFN-β), tumor necrosis factor alpha (TNF-α), and interleukin (IL)-6. In addition, mel significantly attenuated the expression of IkBα, NFkB p65, TRIF and IRF-3, which are involved in TLR4-mediated signaling in OC during ethanol intake. Collectively, our results suggest that mel attenuates the TLR4-induced MyD88- and TRIF-dependent signaling pathways in ethanol-preferring rats with OC.
         datePublished:2015-02-06T00:00:00Z
         dateModified:2025-05-15T00:00:00Z
         pageStart:1
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            Ovarian cancer
            Melatonin
            Inflammation
            TLR4
            MyD88
            TRIF
            Cancer Research
            Oncology
            Surgical Oncology
            Health Promotion and Disease Prevention
            Biomedicine
            general
            Medicine/Public Health
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               name:Luiz Gustavo A Chuffa
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      headline:RETRACTED ARTICLE: Melatonin attenuates the TLR4-mediated inflammatory response through MyD88- and TRIF-dependent signaling pathways in an in vivo model of ovarian cancer
      description:Toll-like receptors (TLRs) are effector molecules expressed on the surface of ovarian cancer (OC) cells, but the functions of the TLR2/TLR4 signaling pathways in these cells remain unclear. Melatonin (mel) acts as an anti-inflammatory factor and has been reported to modulate TLRs in some aggressive tumor cell types. Therefore, we investigated OC and the effect of long-term mel therapy on the signaling pathways mediated by TLR2 and TLR4 via myeloid differentiation factor 88 (MyD88) and toll-like receptor-associated activator of interferon (TRIF) in an ethanol-preferring rat model. To induce OC, the left ovary of animals either consuming 10% (v/v) ethanol or not was injected directly under the bursa with a single dose of 100 μg of 7,12-dimethylbenz(a)anthracene (DMBA) dissolved in 10 μL of sesame oil. The right ovaries were used as sham-surgery controls. After developing OC, half of the animals received i.p. injections of mel (200 μg/100 g b.w./day) for 60 days. Although mel therapy was unable to reduce TLR2 levels, it was able to suppress the OC-associated increase in the levels of the following proteins: TLR4, MyD88, nuclear factor kappa B (NFkB p65), inhibitor of NFkB alpha (IkBα), IkB kinase alpha (IKK-α), TNF receptor-associated factor 6 (TRAF6), TRIF, interferon regulatory factor 3 (IRF3), interferon β (IFN-β), tumor necrosis factor alpha (TNF-α), and interleukin (IL)-6. In addition, mel significantly attenuated the expression of IkBα, NFkB p65, TRIF and IRF-3, which are involved in TLR4-mediated signaling in OC during ethanol intake. Collectively, our results suggest that mel attenuates the TLR4-induced MyD88- and TRIF-dependent signaling pathways in ethanol-preferring rats with OC.
      datePublished:2015-02-06T00:00:00Z
      dateModified:2025-05-15T00:00:00Z
      pageStart:1
      pageEnd:13
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12885-015-1032-4
      keywords:
         Ovarian cancer
         Melatonin
         Inflammation
         TLR4
         MyD88
         TRIF
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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            name:Luiz Gustavo A Chuffa
            affiliation:
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            type:Person
            name:Beatriz A Fioruci-Fontanelli
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                  address:
                     name:Department of Anatomy, Institute of Biosciences, UNESP – Universidade Estadual Paulista, Botucatu, Brazil
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            name:Leonardo O Mendes
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                     type:PostalAddress
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            name:Fábio R Ferreira Seiva
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            name:Marcelo Martinez
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      name:Beatriz A Fioruci-Fontanelli
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            address:
               name:Department of Anatomy, Institute of Biosciences, UNESP – Universidade Estadual Paulista, Botucatu, Brazil
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            address:
               name:Department of Anatomy, Institute of Biosciences, UNESP – Universidade Estadual Paulista, Botucatu, Brazil
               type:PostalAddress
            type:Organization
      name:Fábio R Ferreira Seiva
      affiliation:
            name:UENP - Campus Luiz Meneghel
            address:
               name:Institute of Biology, State University of North of Parana, UENP - Campus Luiz Meneghel, Bandeirantes, Brazil
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            type:Organization
      name:Marcelo Martinez
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            name:UFSCar – Universidade Federal de São Carlos
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               name:Department of Morphology and Pathology, UFSCar – Universidade Federal de São Carlos, São Carlos, Brazil
               type:PostalAddress
            type:Organization
      name:Wagner J Fávaro
      affiliation:
            name:UNICAMP – Universidade de Campinas
            address:
               name:Department of Anatomy, Cell Biology and Physiology and Biophysics, UNICAMP – Universidade de Campinas, Campinas, Brazil
               type:PostalAddress
            type:Organization
      name:Raquel F Domeniconi
      affiliation:
            name:Institute of Biosciences, UNESP – Universidade Estadual Paulista
            address:
               name:Department of Anatomy, Institute of Biosciences, UNESP – Universidade Estadual Paulista, Botucatu, Brazil
               type:PostalAddress
            type:Organization
      name:Patrícia FF Pinheiro
      affiliation:
            name:Institute of Biosciences, UNESP – Universidade Estadual Paulista
            address:
               name:Department of Anatomy, Institute of Biosciences, UNESP – Universidade Estadual Paulista, Botucatu, Brazil
               type:PostalAddress
            type:Organization
      name:Lucilene Delazari dos Santos
      affiliation:
            name:Center for the Study of Venoms and Venomous Animals (CEVAP), UNESP - Univ Estadual Paulista
            address:
               name:Center for the Study of Venoms and Venomous Animals (CEVAP), UNESP - Univ Estadual Paulista, Botucatu, Brazil
               type:PostalAddress
            type:Organization
      name:Francisco Eduardo Martinez
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            name:UFSCar – Universidade Federal de São Carlos
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               name:Department of Morphology and Pathology, UFSCar – Universidade Federal de São Carlos, São Carlos, Brazil
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Anatomy, Institute of Biosciences, UNESP – Universidade Estadual Paulista, Botucatu, Brazil
      name:Department of Anatomy, Institute of Biosciences, UNESP – Universidade Estadual Paulista, Botucatu, Brazil
      name:Department of Anatomy, Institute of Biosciences, UNESP – Universidade Estadual Paulista, Botucatu, Brazil
      name:Institute of Biology, State University of North of Parana, UENP - Campus Luiz Meneghel, Bandeirantes, Brazil
      name:Department of Morphology and Pathology, UFSCar – Universidade Federal de São Carlos, São Carlos, Brazil
      name:Department of Anatomy, Cell Biology and Physiology and Biophysics, UNICAMP – Universidade de Campinas, Campinas, Brazil
      name:Department of Anatomy, Institute of Biosciences, UNESP – Universidade Estadual Paulista, Botucatu, Brazil
      name:Department of Anatomy, Institute of Biosciences, UNESP – Universidade Estadual Paulista, Botucatu, Brazil
      name:Center for the Study of Venoms and Venomous Animals (CEVAP), UNESP - Univ Estadual Paulista, Botucatu, Brazil
      name:Department of Morphology and Pathology, UFSCar – Universidade Federal de São Carlos, São Carlos, Brazil

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