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Proprotein convertase subtilisin/kexin type 6 activates the extracellular signal-regulated kinase 1/2 and Wnt family member 3A pathways and promotes in vitro proliferation, migration and invasion of breast cancer MDA-MB-231 cells

Breast cancer progression results from the acquisition of genetic and epigenetic alterations that promote tumor cell proliferation and survival. Proprotein convertase subtilisin/kexin type 6 (PCSK6) is a proteinase that regulates the proteolytic activity of various precursor proteins as well as prot...

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Detalles Bibliográficos
Autores principales: Wang, Ping, Wang, Feifei, Wang, Lin, Pan, Jihong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6006270/
https://www.ncbi.nlm.nih.gov/pubmed/29928395
http://dx.doi.org/10.3892/ol.2018.8654
Descripción
Sumario:Breast cancer progression results from the acquisition of genetic and epigenetic alterations that promote tumor cell proliferation and survival. Proprotein convertase subtilisin/kexin type 6 (PCSK6) is a proteinase that regulates the proteolytic activity of various precursor proteins as well as protein maturation. PCSK6 also influences cancer cell proliferation, invasion and migration. Therefore, to investigate the effects of PCSK6 in breast cancer, human breast cancer MDA-MB-231 cells were treated with recombinant human PCSK6 in vitro. Treatment with recombinant PCSK6 significantly increased the proliferation, invasion and migration abilities of MDA-MB-231 cells. In addition, PCSK6 treatment reduced cell cycle arrest and prevented apoptosis of MDA-MB-231 cells. This provides further support for the hypothesis that PCSK6 serves a role in promoting tumor cell proliferation. PCSK6 treatment also increased the expression of phosphorylated extracellular signal-regulated kinase 1/2 and Wnt family member 3A, suggesting that these pathways are activated by PCSK6. The results of the present study suggested that PCSK6 may promote the proliferation of breast cancer MDA-MB-231 cells by disturbing cell cycle arrest via the mitogen-activated protein kinase pathway. Therefore, PCSK6 may be a potential therapeutic target for breast cancer.