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Type: Artigo
Title: Endostatin induces proliferation of oral carcinoma cells but its effect on invasion is modified by the tumor microenvironment
Author: Alahuhta, Ilkka
Aikio, Mari
Vayrynen, Otto
Nurmenniemi, Sini
Suojanen, Juho
Teppo, Susanna
Pihlajaniemi, Taina
Heljasvaara, Ritva
Salo, Tuula
Nyberg, Pia
Abstract: The turnover of extracellular matrix liberates various cryptic molecules with novel biological activities. Endostatin is an endogenous angiogenesis inhibitor that is derived from the non-collagenous domain of collagen XVIII. Although there are a large number of studies on its anti-tumor effects, the molecular mechanisms are not yet completely understood, and the reasons why endostatin has not been successful in clinical trials are unclear. Research has mostly focused on its anti-angiogenic effect in tumors. Here, we aimed to elucidate how endostatin affects the behavior of aggressive tongue HSC-3 carcinoma cells that were transfected to overproduce endostatin. Endostatin inhibited the invasion of HSC-3 cells in a 3D collagen-fibroblast model. However, it had no effect on invasion in a human myoma organotypic model, which lacks vital fibroblasts. Recombinant endostatin was able to reduce the Transwell migration of normal fibroblasts, but had no effect on carcinoma associated fibroblasts. Surprisingly, endostatin increased the proliferation and decreased the apoptosis of cancer cells in organotypic models. Also subcutaneous tumors overproducing endostatin grew bigger, but showed less local invasion in nude mice xenografts. We conclude that endostatin affects directly to HSC-3 cells increasing their proliferation, but its net effect on cancer invasion seem to depend on the cellular composition and interactions of tumor microenvironment
Subject: Matriz extracelular
Células cancerosas
Country: Estados Unidos
Editor: Elsevier
Rights: Fechado
Identifier DOI: 10.1016/j.yexcr.2015.06.012
Date Issue: 2015
Appears in Collections:FOP - Artigos e Outros Documentos

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