WCRB2014 POSTER PRESENTATIONS (1) (335 abstracts)
TLR4-mediated signaling pathway is modulated by melatonin through MyD88-dependent pathway in ovarian carcinoma of ethanol-consuming rats
Luiz Gustavo Chuffa 1 , Beatriz Fioruci-Fontanelli 1 , Leonardo Mendes 1 , Patrícia Fernanda Pinheiro 1 , Marcelo Martinez 2 & FranciscoEduardo Martinez 1
1Botucatu, Brazil; 2Ufscar, São Carlos, Brazil.
Introduction: Toll-like receptors (TLRs) are active molecules expressed on the surface of ovarian cancer (OC) cells, but the consequences of TLR2/TLR4 signaling pathways in these cells remain unclear. Because melatonin (mel) act as an immunomodulatory hormone and has been reported to modulate TLRs in some aggressive tumor cells, we investigated the effective role of long-term mel therapy on TLR2- and TLR4-mediated molecule myeloid differentiation factor 88 (MyD88)-dependent signaling pathway in OC of ethanol-preferring rats.
Materials and methods: After developing OC, half of the animals received i.p. injections of mel (200 μg/100 g BW per day) for 60 days. Four experimental groups were established: Group C, rats bearing OC; Group EtOH+C, rats voluntarily consuming 10% (v/v) EtOH and bearing OC; Group C+M, rats bearing OC and receiving mel; and Group EtOH+C+M, rats with OC consuming EtOH and receiving mel. The target proteins/factors were investigated through immunohistochemistry and western blot analysis.
Results and discussion: While mel therapy was unable to reduce TLR2 levels, it was able to suppress TLR4, MyD88, inhibitor of nuclear factor kappa beta kinase alpha (IKKα), nuclear factor kappa B (NFkB p65), and inhibitor of NFkB (IkBα) in OC. In addition, mel significantly attenuated the elevation of IkBα and NFkB p65 during ethanol intake, which were involved in TLR4-mediated signaling in OC. Together, our results suggest that mel modulates TLR4-induced MyD88-dependent signaling pathway in OC of ethanol-preferring rats.
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