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Laminin‐derived peptide C16 regulates Tks expression and reactive oxygen species generation in human prostate cancer cells
Author(s) -
CairesdosSantos Livia,
da Silva Suély V.,
Smuczek Basilio,
Siqueira Adriane S.,
Cruz Karen S. P.,
Barbuto José Alexandre M.,
Augusto Taize M.,
Freitas Vanessa M.,
Carvalho Hernandes F.,
Jaeger Ruy G.
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28997
Subject(s) - du145 , invadopodia , reactive oxygen species , cancer cell , cortactin , colocalization , microbiology and biotechnology , laminin , chemistry , matrix metalloproteinase , flow cytometry , cancer , extracellular matrix , biochemistry , biology , cell , genetics , cytoskeleton , lncap
Laminin peptides influence cancer biology. We investigated the role of a laminin‐derived peptide C16 regulating invadopodia molecules in human prostate cancer cells (DU145). C16 augmented invadopodia activity of DU145 cells, and stimulated expression Tks4, Tks5, cortactin, and membrane‐type matrix metalloproteinase 1. Reactive oxygen species generation is also related to invadopodia formation. This prompted us to address whether C16 would induce reactive oxygen species generation in DU145 cells. Quantitative fluorescence and flow cytometry showed that the peptide C16 increased reactive oxygen species in DU145 cells. Furthermore, significant colocalization between Tks5 and reactive oxygen species was observed in C16‐treated cells. Results suggested that the peptide C16 increased Tks5 and reactive oxygen species in prostate cancer cells. The role of C16 increasing Tks and reactive oxygen species are novel findings on invadopodia activity.