MAPK7 Gene Controls Proliferation, Migration and Cell Invasion in Osteosarcoma

MAPK7 Gene Controls Proliferation, Migration and Cell Invasion in Osteosarcoma

Author Gamba, Francine Tesser Autor UNIFESP Google Scholar
Lopes, Luana Joyce da Silva Autor UNIFESP Google Scholar
Petrilli, Antonio Sergio Autor UNIFESP Google Scholar
Toledo, Silvia Regina Caminada de Autor UNIFESP Google Scholar
Abstract Osteosarcomas (OS) are the most common malignant bone tumors, and the identification of useful tumor biomarkers and target proteins is required to predict the clinical outcome of patients and therapeutic response as well as to develop novel therapeutic strategies. In our previous study, MAPK7 has been identified as a candidate oncogene, and a promising prognostic marker for OS. Sequential activation of protein kinases within the mitogen-activated protein kinase (MAPK) cascades is a common mechanism of signal transduction in many cellular processes. In this study, we investigated the behavior of MAPK7 gene in OS cell lines. Technical viability, proliferation, migration, invasion, and apoptosis were used to evaluate the function of the MAPK7 gene. We evaluated the behavior of the OS cells with MAPK7 gene silenced, not silenced, and exposed to the main chemotherapy drugs used in OS treatment. We found that silenced MAPK7 gene is effective at suppressing cell proliferation, inhibiting cell migration, and invasion. Furthermore, MAPK7 is an important activator of transcription factors and is the main expression modulator of other key genes in the MAPK pathway. In summary, our study suggests that MAPK7 might be a promising therapeutic target for OS. (C) 2015 Wiley Periodicals, Inc.
Keywords MAP kinase signaling system
osteosarcoma
therapeutic target
biological tumor marker
MAPK7
xmlui.dri2xhtml.METS-1.0.item-coverage Hoboken
Language English
Sponsor Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Pediatric Oncology Institute IOP-GRAACC/UNIFESP
Grant number FAPESP: 2010/10782-8
FAPESP: 2011/10459-5
Date 2016
Published in Molecular Carcinogenesis. Hoboken, v. 55, n. 11, p. 1700-1713, 2016.
ISSN 0899-1987 (Sherpa/Romeo, impact factor)
Publisher Wiley-Blackwell
Extent 1700-1713
Origin http://dx.doi.org/10.1002/mc.22420
Access rights Closed access
Type Article
Web of Science ID WOS:000387853200018
URI https://repositorio.unifesp.br/handle/11600/56814

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