作者: IF Bambang , YK Lee , DR Richardson , D Zhang , None
DOI: 10.1038/ONC.2012.149
关键词:
摘要: The epithelial-mesenchymal transition (EMT) correlates with disruption of cell-cell adhesion, loss cell polarity and development epithelial malignancy. Identifying novel molecules that inhibit EMT has profound potential for developing mechanism-based therapeutics. We previously demonstrated the endoplasmic reticulum protein 29 (ERp29) is a factor can drive mesenchymal-epithelial (MET) induce growth arrest in MDA-MB-231 cells. Here, we show ERp29 an important molecule establishing integrity during MET. demonstrate regulates MET context-dependent manner. overexpression induced complete mesenchymal cells through downregulating expression transcriptional repressors (for example, Slug, Snai1, ZEB2 Twist) E-cadherin. In contrast, induces incomplete basal-like BT549 which EMT-related markers vimentin; cytokeratin 19 (CK19) E-cadherin) E-cadherin were not altered. However, both cell-types resulted filamentous stress fibers, formation cortical actin restoration phenotype. Mechanistic studies revealed upregulated TJ proteins (zonula-occludens-1 (ZO-1) occludin) core apical-basal (Par3 Scribble) at membrane to enhance contact polarization. Knockdown MCF-7 decreased these proteins, leading adhesion. Taken together, breast cancer