Evaluation of melatonin treatment in primary culture of canine mammary tumors

Mammary neoplasias are the most common tumors observed in female dogs. Identification of these tumors is valuable in order to identify beneficial therapeutic agents as alternative treatments for this tumor type. Oral administration of melatonin appears to exert an oncostatic effect on mammary neopla...

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Veröffentlicht in:Oncology reports 2015-01, Vol.33 (1), p.311-319
Hauptverfasser: LOPES, JULIANA RAMOS, MASCHIO, LARISSA BAZELA, JARDIM-PERASSI, BRUNA VICTORASSO, MOSCHETTA, MARINA GOBBE, FERREIRA, LÍVIA CARVALHO, MARTINS, GUSTAVO RODRIGUES, GELALETI, GABRIELA BOTTARO, DE CAMPOS ZUCCARI, DEBORA APARECIDA PIRES
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container_issue 1
container_start_page 311
container_title Oncology reports
container_volume 33
creator LOPES, JULIANA RAMOS
MASCHIO, LARISSA BAZELA
JARDIM-PERASSI, BRUNA VICTORASSO
MOSCHETTA, MARINA GOBBE
FERREIRA, LÍVIA CARVALHO
MARTINS, GUSTAVO RODRIGUES
GELALETI, GABRIELA BOTTARO
DE CAMPOS ZUCCARI, DEBORA APARECIDA PIRES
description Mammary neoplasias are the most common tumors observed in female dogs. Identification of these tumors is valuable in order to identify beneficial therapeutic agents as alternative treatments for this tumor type. Oral administration of melatonin appears to exert an oncostatic effect on mammary neoplasia and may have a possible mechanism of action through its interaction with estrogen receptors on epithelial cells. Hence, we analyzed the potential therapeutic value of melatonin in tumors that are estrogen-dependent or -independent, and established a relationship of its action with the expression of the melatonin receptors MT1 and MT2. Furthermore, we analyzed the rate of cell proliferation and apoptosis after treatment with melatonin. Cell cultures were performed using 10 canine mammary tumor fragments and were divided into estrogen receptor (ER)-positive and ER-negative tumors. The results showed that both ER-positive and ER-negative tumors had decreased cell viability and proliferation after treatment with melatonin (p
doi_str_mv 10.3892/or.2014.3596
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Identification of these tumors is valuable in order to identify beneficial therapeutic agents as alternative treatments for this tumor type. Oral administration of melatonin appears to exert an oncostatic effect on mammary neoplasia and may have a possible mechanism of action through its interaction with estrogen receptors on epithelial cells. Hence, we analyzed the potential therapeutic value of melatonin in tumors that are estrogen-dependent or -independent, and established a relationship of its action with the expression of the melatonin receptors MT1 and MT2. Furthermore, we analyzed the rate of cell proliferation and apoptosis after treatment with melatonin. Cell cultures were performed using 10 canine mammary tumor fragments and were divided into estrogen receptor (ER)-positive and ER-negative tumors. The results showed that both ER-positive and ER-negative tumors had decreased cell viability and proliferation after treatment with melatonin (p&lt;0.05), although treatment was more effective in the ER-positive tumors. Analysis of the relative expression of the MT1 and MT2 genes by quantitative PCR was performed and the data were compared with the expression of ER in 24 canine mammary tumors and the cellular response to melatonin in 10 samples. MT1 was overexpressed in ER-positive tumors (p&lt;0.05), whereas MT2 was not expressed. Furthermore, melatonin treatment in ER-positive tumors showed an efficient oncostatic effect by inhibiting cell viability and proliferation and inducing apoptosis. These results suggest that melatonin decreased neoplastic mammary cell proliferation and viability and induced apoptosis, with greater efficacy in ER-positive tumors that have a high expression of melatonin receptor MT1. 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Identification of these tumors is valuable in order to identify beneficial therapeutic agents as alternative treatments for this tumor type. Oral administration of melatonin appears to exert an oncostatic effect on mammary neoplasia and may have a possible mechanism of action through its interaction with estrogen receptors on epithelial cells. Hence, we analyzed the potential therapeutic value of melatonin in tumors that are estrogen-dependent or -independent, and established a relationship of its action with the expression of the melatonin receptors MT1 and MT2. Furthermore, we analyzed the rate of cell proliferation and apoptosis after treatment with melatonin. Cell cultures were performed using 10 canine mammary tumor fragments and were divided into estrogen receptor (ER)-positive and ER-negative tumors. The results showed that both ER-positive and ER-negative tumors had decreased cell viability and proliferation after treatment with melatonin (p&lt;0.05), although treatment was more effective in the ER-positive tumors. Analysis of the relative expression of the MT1 and MT2 genes by quantitative PCR was performed and the data were compared with the expression of ER in 24 canine mammary tumors and the cellular response to melatonin in 10 samples. MT1 was overexpressed in ER-positive tumors (p&lt;0.05), whereas MT2 was not expressed. Furthermore, melatonin treatment in ER-positive tumors showed an efficient oncostatic effect by inhibiting cell viability and proliferation and inducing apoptosis. These results suggest that melatonin decreased neoplastic mammary cell proliferation and viability and induced apoptosis, with greater efficacy in ER-positive tumors that have a high expression of melatonin receptor MT1. 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Identification of these tumors is valuable in order to identify beneficial therapeutic agents as alternative treatments for this tumor type. Oral administration of melatonin appears to exert an oncostatic effect on mammary neoplasia and may have a possible mechanism of action through its interaction with estrogen receptors on epithelial cells. Hence, we analyzed the potential therapeutic value of melatonin in tumors that are estrogen-dependent or -independent, and established a relationship of its action with the expression of the melatonin receptors MT1 and MT2. Furthermore, we analyzed the rate of cell proliferation and apoptosis after treatment with melatonin. Cell cultures were performed using 10 canine mammary tumor fragments and were divided into estrogen receptor (ER)-positive and ER-negative tumors. 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This is a strong evidence for the use of melatonin as a therapeutic agent for estrogen-dependent canine mammary tumors.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25384569</pmid><doi>10.3892/or.2014.3596</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Analysis
Animals
Antineoplastic Agents - pharmacology
Apoptosis
Breast cancer
Cell growth
Cell Proliferation - drug effects
Cell Survival - drug effects
Dog Diseases - drug therapy
Dog Diseases - metabolism
Dogs
Drug Screening Assays, Antitumor
Drug therapy
Estrogen
estrogen receptor
Estrogens
Female
Gene Expression
Genetic aspects
Health aspects
immunocytochemistry
Lymphatic system
Mammary Neoplasms, Animal - drug therapy
Mammary Neoplasms, Animal - metabolism
Medical prognosis
Melatonin
Melatonin - pharmacology
Metastasis
MT1
MT2
Physiological aspects
Primary Cell Culture
Receptor, Melatonin, MT1 - genetics
Receptor, Melatonin, MT1 - metabolism
Receptor, Melatonin, MT2 - genetics
Receptor, Melatonin, MT2 - metabolism
Rodents
Tumor Cells, Cultured
Tumors
title Evaluation of melatonin treatment in primary culture of canine mammary tumors
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