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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Apoptosis is triggered by melatonin in an in vivo model of ovarian carcinoma

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Chuffa, Luiz Gustavo A. [1] ; Alves, Michelly S. [1] ; Martinez, Marcelo [2] ; Camargo, Isabel Cristina C. [3] ; Pinheiro, Patricia F. F. [1] ; Domeniconi, Raquel F. [1] ; Junior, Luiz Antonio L. [1] ; Martinez, Francisco Eduardo [1]
Total Authors: 8
[1] UNESP Univ Estadual Paulista, Dept Anat, Inst Biosci Botucatu, BR-510 Sao Paulo - Brazil
[2] UFSCar Univ Fed Sao Carlos, Dept Morphol & Pathol, BR-13565905 Sao Paulo - Brazil
[3] UNESP Univ Estadual Paulista, Fac Sci & Letters, Dept Biol Sci, BR-19806900 Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Endocrine-Related Cancer; v. 23, n. 2, p. 65-76, FEB 2016.
Web of Science Citations: 23

Apoptosis plays an important role in the treatment of cancer, and targeting apoptosis-related molecules in ovarian cancer (OC) is of great therapeutic value. Melatonin (Mel) is an indoleamine displaying several anti-cancer properties and has been reported to modulate apoptosis signaling in multiple tumor subtypes. We investigated OC and the role of Mel therapy on the pro-apoptotic (p53, BAX, caspase-3, and cleaved caspase-3) and anti-apoptotic (Bcl-2 and survivin) proteins in an ethanol (EtOH)-preferring rat model. To induce OC, the left ovary was injected directly with a single dose of 100 mu g 7,12-dimethylbenz(a) anthracene dissolved in 10 mu l of sesame oil under the bursa. Right ovaries were used as sham-surgery controls. After developing OC, half of the animals received i.p. injections of Mel (200 mu g/100 g BW per day) for 60 days. Body weight gain, EtOH consumption, and energy intake were unaffected by the treatments. Interestingly, absolute and relative OC masses showed a significant reduction after Mel therapy, regardless of EtOH consumption. To accomplish OC-related apoptosis, we first observed that p53, BAX, caspase-3, and cleaved caspase-3 were downregulated in OC tissue while Bcl-2 and survivin were overexpressed. Notably, Mel therapy and EtOH intake promoted apoptosis along with the upregulation of p53, BAX, and cleaved caspase-3. Fragmentation of DNA observed by TUNEL-positive nuclei was also enhanced following Mel treatment. In addition, Bcl-2 was downregulated by the EtOH intake and lower survivin levels were observed after Mel therapy. Taken together, these results suggest that Mel induce apoptosis in OC cells of EtOH-preferring animals. (AU)

FAPESP's process: 14/05196-3 - Induction of ovarian tumor and the influence of melatonin therapy on the apoptosis of UChB rats
Grantee:Michelly da Silva Alves
Support Opportunities: Scholarships in Brazil - Scientific Initiation
FAPESP's process: 13/02466-7 - Induction of ovarian tumor and influence of melatonin on inflammatory signaling pathway mediated by Toll-like receptor 4 in UChB rats
Grantee:Luiz Gustavo de Almeida Chuffa
Support Opportunities: Regular Research Grants