Laminin-111 derived peptides AG73 and C16 regulate invadopodia activity of a human adenoid cystic carcinoma cell line.
作者： Camila F Nascimento , Adriane S de Siqueira , João JV Pinheiro , Vanessa M Freitas , Ruy G Jaeger
DOI: 10.1016/J.YEXCR.2011.08.022
关键词:
摘要: Adenoid cystic carcinoma is a frequently occurring malignant salivary gland neoplasm with high level of recurrence and distant metastasis long time after treatment. Metastatic tumor cells that actively migrate invade surrounding tissues rely on invadopodia to degrade extracellular matrix (ECM) barriers. Invadopodia are actin-rich membrane protrusions localize enzymes required for ECM degradation. Breakdown macromolecules releases fragments bioactive peptides. We have already demonstrated laminin-111 its derived peptides regulate migration, invasion protease activity adenocarcinoma cells. Here we addressed the role AG73 C16 in (CAC2) from human adenoid carcinoma. CAC2 were treated by C16, subjected fluorescent gelatin substrate degradation assay. In this assay areas appear as black dots background. Both significantly increased formation compared controls. analyzed putative receptors signaling pathways related peptide effects. β1 integrin silencing siRNA decreased AG73- C16-induced invadopodia. Furthermore inhibition Rac1 ERK both C16- AG73-related activities. propose increase through integrin. ERK1/2 would transduce signals generated
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