Carneiro Bruna Ribeiro, Pernambuco Filho Paulo Castanho A, Mesquita Ana Paula de Sousa, da Silva Douglas Santos, Pinhal Maria Aparecida S, Nader Helena B, Lopes Carla Cristina
Departamento de Ciências Biológicas, Universidade Federal de São Paulo, Diadema, SP, Brazil; Departamento de Bioquímica, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Departamento de Bioquímica, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
PLoS One. 2014 Dec 30;9(12):e116001. doi: 10.1371/journal.pone.0116001. eCollection 2014.
Anoikis is a programmed cell death induced upon cell detachment from extracellular matrix, behaving as a critical mechanism in preventing adherent-independent cell growth and attachment to an inappropriate matrix, thus avoiding colonization of distant organs. Cell adhesion plays an important role in neoplastic transformation. Tumors produce several molecules that facilitate their proliferation, invasion and maintenance, especially proteoglycans. The syndecan-4, a heparan sulfate proteoglycan, can act as a co-receptor of growth factors and proteins of the extracellular matrix by increasing the affinity of adhesion molecules to their specific receptors. It participates together with integrins in cell adhesion at focal contacts connecting the extracellular matrix to the cytoskeleton. Changes in the expression of syndecan-4 have been observed in tumor cells, indicating its involvement in cancer. This study investigates the role of syndecan-4 in the process of anoikis and cell transformation. Endothelial cells were submitted to sequential cycles of forced anchorage impediment and distinct lineages were obtained. Anoikis-resistant endothelial cells display morphological alterations, high rate of proliferation, poor adhesion to fibronectin, laminin and collagen IV and deregulation of the cell cycle, becoming less serum-dependent. Furthermore, anoikis-resistant cell lines display a high invasive potential and a low rate of apoptosis. This is accompanied by an increase in the levels of heparan sulfate and chondroitin sulfate as well as by changes in the expression of syndecan-4 and heparanase. These results indicate that syndecan-4 plays a important role in acquisition of anoikis resistance and that the conferral of anoikis resistance may suffice to transform endothelial cells.
失巢凋亡是细胞从细胞外基质脱离后引发的程序性细胞死亡,是防止非贴壁依赖性细胞生长以及避免细胞附着于不适当基质从而防止远处器官定植的关键机制。细胞黏附在肿瘤转化过程中起着重要作用。肿瘤会产生多种促进其增殖、侵袭和维持的分子,尤其是蛋白聚糖。硫酸乙酰肝素蛋白聚糖Syndecan-4可通过增加黏附分子与其特异性受体的亲和力,充当生长因子和细胞外基质蛋白的共受体。它与整合素共同参与细胞在将细胞外基质与细胞骨架相连的黏着斑处的黏附。在肿瘤细胞中已观察到Syndecan-4表达的变化,表明其与癌症有关。本研究调查了Syndecan-4在失巢凋亡和细胞转化过程中的作用。对内皮细胞进行连续的强制锚定阻碍循环,获得了不同的细胞系。抗失巢凋亡的内皮细胞表现出形态改变、高增殖率、对纤连蛋白、层粘连蛋白和IV型胶原的黏附性差以及细胞周期失调,对血清的依赖性降低。此外,抗失巢凋亡细胞系具有高侵袭潜力和低凋亡率。这伴随着硫酸乙酰肝素和硫酸软骨素水平的增加以及Syndecan-4和乙酰肝素酶表达的变化。这些结果表明,Syndecan-4在获得抗失巢凋亡能力中起重要作用,并且赋予抗失巢凋亡能力可能足以使内皮细胞发生转化。