Laboratorio Of Investigacao Molecular Do Cancer Limc

São José do Rio Preto, Brazil

Laboratorio Of Investigacao Molecular Do Cancer Limc

São José do Rio Preto, Brazil
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Gelaleti G.B.,São Paulo State University | Gelaleti G.B.,Laboratorio Of Investigacao Molecular Do Cancer Limc | Borin T.F.,University of Georgia | Maschio-Signorini L.B.,Laboratorio Of Investigacao Molecular Do Cancer Limc | And 7 more authors.
Life Sciences | Year: 2017

Mammary tumorigenesis can be modulated by melatonin, which has oncostatic action mediated by multiple mechanisms, including the inhibition of the activity of transcription factors such as NF-κB and modulation of interleukins (ILs) expression. IL-25 is an active cytokine that induces apoptosis in tumor cells due to differential expression of its receptor (IL-17RB). IL-17B competes with IL-25 for binding to IL-17RB in tumor cells, promoting tumorigenesis. This study purpose is to address the possibility of engaging IL-25/IL-17RB signaling to enhance the effect of melatonin on breast cancer cells. Breast cancer cell lines were cultured monolayers and 3D structures and treated with melatonin, IL-25, siIL-17B, each alone or in combination. Cell viability, gene and protein expression of caspase-3, cleaved caspase-3 and VEGF-A were performed by qPCR and immunofluorescence. In addition, an apoptosis membrane array was performed in metastatic cells. Treatments with melatonin and IL-25 significantly reduced tumor cells viability at 1 mM and 1 ng/mL, respectively, but did not alter cell viability of a non-tumorigenic epithelial cell line (MCF-10A). All treatments, alone and combined, significantly increased cleaved caspase-3 in tumor cells grown as monolayers and 3D structures (p < 0.05). Semi-quantitative analysis of apoptosis pathway proteins showed an increase of CYTO-C, DR6, IGFBP-3, IGFBP-5, IGFPB-6, IGF-1, IGF-1R, Livin, P21, P53, TNFRII, XIAP and hTRA proteins and reduction of caspase-3 (p < 0.05) after melatonin treatment. All treatments reduced VEGF-A protein expression in tumor cells (p < 0.05). Our results suggest therapeutic potential, with oncostatic effectiveness, pro-apoptotic and anti-angiogenic properties for melatonin and IL-25-driven signaling in breast cancer cells. © 2016 Elsevier Inc.


Bottino J.,Laboratorio Of Investigacao Molecular Do Cancer Limc | Gelaleti G.B.,Laboratorio Of Investigacao Molecular Do Cancer Limc | Gelaleti G.B.,São Paulo State University | Maschio L.B.,Laboratorio Of Investigacao Molecular Do Cancer Limc | And 5 more authors.
Acta Histochemica | Year: 2014

Breast cancer is the most common tumor in women and it has high mortality mainly due to the occurrence of tumor metastasis. Both the processes of cell migration and anchorage to the substrate are essential for the development of metastasis. These processes occur by rearrangements of the actin cytoskeleton, regulated by Rho-associated protein kinase 1 (ROCK-1). The degradation of the extracellular matrix, influenced by metalloproteinase 9 (MMP-9) also exerts greater cell invasiveness. The present study evaluated the ROCK-1 and MMP-9 proteins using an immunohistochemical method through the selection of invasive ductal breast carcinoma. The protein expression was correlated to clinicopathological parameters and overall survival of the patients. High expression of the ROCK-1 protein was correlated statistically to the status of lymph nodes (. p=. 0.007) and showed variable expression in different clinical stages of the tumor. MMP-9 showed a strong immunostaining in patients with metastasis that had died, whereas there was no marker in normal breast tissues. In addition, 46.6% of patients classified as poor prognosis showed high expression of ROCK-1 and MMP-9 protein and another 40.0% just showed high expression of MMP-9. Thus, the differential expression of ROCK-1 and MMP-9 proteins suggests their potential use as prognostic markers in breast cancer. © 2014 Elsevier GmbH.

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