EMT in Metastasis: Finding the Right Balance

Hin Ching Lo; Xiang H-F Zhang

doi:10.1016/j.devcel.2018.05.033

EMT in Metastasis: Finding the Right Balance

Dev Cell. 2018 Jun 18;45(6):663-665. doi: 10.1016/j.devcel.2018.05.033.

Authors

Hin Ching Lo¹, Xiang H-F Zhang²

Affiliations

¹ Lester and Sue Smith Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Dan L. Duncan Cancer Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Graduate Program in Integrative Molecular and Biomedical Sciences, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
² Lester and Sue Smith Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Dan L. Duncan Cancer Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; McNair Medical Institute, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA. Electronic address: xiangz@bcm.edu.

PMID: 29920271
DOI: 10.1016/j.devcel.2018.05.033

Abstract

The epithelial-to-mesenchymal transition (EMT) is a key driver of cancer metastasis. In this issue of Developmental Cell, Aiello et al. (2018) demonstrate that an EMT mechanism involving protein internalization impacts cell migration, while Reichert et al. (2018) identify epithelial plasticity as a determinant of metastatic organotropism in pancreatic cancer.

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MeSH terms

Cell Movement
Epithelial-Mesenchymal Transition*
Humans
Neoplasm Metastasis
Pancreatic Neoplasms*