Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 Mar;12(1):12-20.
doi: 10.5808/GI.2014.12.1.12. Epub 2014 Mar 31.

Membrane Proteins Involved in Epithelial-Mesenchymal Transition and Tumor Invasion: Studies on TMPRSS4 and TM4SF5

Semi Kim  1 , Jung Weon Lee  2
Affiliations
Review

Membrane Proteins Involved in Epithelial-Mesenchymal Transition and Tumor Invasion: Studies on TMPRSS4 and TM4SF5

Semi Kim et al. Genomics Inform. 2014 Mar.

Abstract

The epithelial-mesenchymal transition (EMT) is one mechanism by which cells with mesenchymal features can be generated and is a fundamental event in morphogenesis. Recently, invasion and metastasis of cancer cells from the primary tumor are now thought to be initiated by the developmental process termed the EMT, whereby epithelial cells lose cell polarity and cell-cell interactions, and gain mesenchymal phenotypes with increased migratory and invasive properties. The EMT is believed to be an important step in metastasis and is implicated in cancer progression, although the influence of the EMT in clinical specimens has been debated. This review presents the recent results of two cell surface proteins, the functions and underlying mechanisms of which have recently begun to be demonstrated, as novel regulators of the molecular networks that induce the EMT and cancer progression.

Keywords: TM4SF5; TMPRSS4; epithelial-mesenchymal transition; invasion; membrane proteins.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Cellular functions of TMPRSS4. ENaC, epithelial sodium channel; uPA, urokinase plasminogen activator; EMT, epithelialmesenchymal transition.
Fig. 2
Fig. 2
TM4SF5-mediated epithelial-mesenchymal transition (EMT) is involved in diverse cellular functions, leading to liver tumorigenesis and maintenance in addition to developmental processes.
See this image and copyright information in PMC

References

    1. Kalluri R. EMT: when epithelial cells decide to become mesenchymal-like cells. J Clin Invest. 2009;119:1417–1419. - PMC - PubMed
    1. Thiery JP, Acloque H, Huang RY, Nieto MA. Epithelial-mesenchymal transitions in development and disease. Cell. 2009;139:871–890. - PubMed
    1. Thiery JP, Sleeman JP. Complex networks orchestrate epithelial-mesenchymal transitions. Nat Rev Mol Cell Biol. 2006;7:131–142. - PubMed
    1. Yang J, Weinberg RA. Epithelial-mesenchymal transition: at the crossroads of development and tumor metastasis. Dev Cell. 2008;14:818–829. - PubMed
    1. Peinado H, Olmeda D, Cano A. Snail, Zeb and bHLH factors in tumour progression: an alliance against the epithelial phenotype? Nat Rev Cancer. 2007;7:415–428. - PubMed

LinkOut - more resources