Marina Gobbe Moschetta-Pinheiro

Prof. Dr. Marina Gobbe Moschetta-Pinheiro


Research Focus & Metrics

Academic Career Length

10Years (2017-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 August 2017 in Life Sciences
Verified
Journal Article
Closed access
GGGabriela Bottaro Gelaleti
Gabriela Bottaro Gelaleti
TBThaiz Borin
Thaiz Borin
LMLarissa Bazela Maschio-Signorini
Larissa Bazela Maschio-Signorini
MMMarina Gobbe Moschetta-Pinheiro
Marina Gobbe Moschetta-Pinheiro
BJBruna Victorasso Jardim-Perassi
Bruna Victorasso Jardim-Perassi
Debora Aparecida Pires Campos ZuccariDebora Aparecida Pires Campos Zuccari
Debora Aparecida Pires Campos Zuccari

21 September 2021 in Veterinary and Comparative Oncology
Verified
Journal Article
Closed access
JOJéssica Rodrigues de Oliveira
Jéssica Rodrigues de Oliveira
JCJucimara Colombo
Jucimara Colombo
FGFrancine Moraes Gonçalves
Francine Moraes Gonçalves
Lucas Amoroso Lopes de CarvalhoLucas Amoroso Lopes de Carvalho
Lucas Amoroso Lopes de Carvalho
DCDouglas Santos Costa
Douglas Santos Costa
Debora Aparecida Pires Campos ZuccariDebora Aparecida Pires Campos Zuccari
Debora Aparecida Pires Campos Zuccari

12 May 2022 in Anti-Cancer Agents in Medicinal Chemistry
Verified
Journal Article
Closed access
PDF file
MMMarina Gobbe Moschetta-Pinheiro
Marina Gobbe Moschetta-Pinheiro
JCJucimara Colombo
Jucimara Colombo
MTMurillo de Souza Tuckumantel
Murillo de Souza Tuckumantel
GRGabriela Karam Rebolho
Gabriela Karam Rebolho
Debora Aparecida Pires Campos ZuccariDebora Aparecida Pires Campos Zuccari
Debora Aparecida Pires Campos Zuccari
Background: The most aggressive breast cancer is the triple negative histological type, and the gold standard for its treatment is platinum salts, such as carboplatin. Due to high recurrence, there is a need to test new drugs, such as PARP inhibitors (PARPi), that induce lethality in cells with DNA damage. Olaparib is a PARPi, already used in some tumors but not tested in canine species. Thus, the aim of this study was to demonstrate the efficacy of olaparib in inhibiting DNA repair and control disease progression by decreasing the migration capacity of mammary tumor cells. Methods: The cell lines CF41.Mg and MDA-MB-468 were cultured and MTT was performed to define the best dose of carboplatin. Next, the cells were treated with 10 μM carboplatin, olaparib, and with a combination of both for 24 hours. PARP-1 protein and gene expression were evaluated by immunofluorescence, western blotting, and qRT-PCR, respectively. The analysis of cell migration was performed in transwell chambers. Results: For CF41.Mg and MDA-MB-468 cell lines, there was a decrease in PARP-1 protein and gene expression after treatment with carboplatin, olaparib, and both in combination compared to the group without treatment (control) (p<0.05). Moreover, in both lines, a reduction in invasion rate was observed after treatment with carboplatin, olaparib and when combined, compared to the control group (p<0.05). Conclusion: Our data suggest that carboplatin and olaparib were able to block DNA repair and control the cancer invasion, especially when used in combination. The results with olaparib in the canine line are unpublished. The olaparib should be a possible agent against human breast cancer and canine mammary tumors.