Related Experiment Video
Updated: May 4, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Exo70 isoform switching upon epithelial-mesenchymal transition mediates cancer cell invasion
Hezhe Lu1, Jianglan Liu1, Shujing Liu2
1Department of Biology, School of Arts and Sciences, University of Pennsylvania, Philadelphia, PA 19104, USA.
Abstract:
Epithelial-mesenchymal transition (EMT) is an important developmental process hijacked by cancer cells for their dissemination. Here, we show that Exo70, a component of the exocyst complex, undergoes isoform switching mediated by ESRP1, a pre-mRNA splicing factor that regulates EMT. Expression of the epithelial isoform of Exo70 affects the levels of key EMT transcriptional regulators such as Snail and ZEB2 and is sufficient to drive the transition to epithelial phenotypes. Differential Exo70 isoform expression in human tumors correlates with cancer progression, and increased expression of the epithelial isoform of Exo70 inhibits tumor metastasis in mice. At the molecular level, the mesenchymal-but not the epithelial-isoform of Exo70 interacts with the Arp2/3 complex and stimulates actin polymerization for tumor invasion. Our findings provide a mechanism by which the exocyst function and actin dynamics are modulated for EMT and tumor invasion.
Related Concept Videos
Cancer Cell Migration through Invadopodia
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Cadherins in Tissue Organization
Cell Sorting During Development
Cell sorting plays an...
The Tumor Microenvironment
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal
Mitogens and the Cell Cycle

