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Open AccessArticle

P120 Catenin Isoforms Differentially Associate with Breast Cancer Invasion and Metastasis

1
Department of Cell Biology, Radboud Institute for Molecular Life Sciences (RIMLS), Radboud University Medical Center, 6525 GA Nijmegen, The Netherlands
2
Radiotherapy & OncoImmunology Laboratory, Department of Radiation Oncology, Radboud Institute for Molecular Life Sciences (RIMLS), Radboud University Medical Center, 6525 GA Nijmegen, The Netherlands
3
Department of Laboratory Medicine, Radboud University Medical Center, 6525 GA Nijmegen, The Netherlands
4
Cancer Genomic Centre, University Medical Center Utrecht, 3584 CG Utrecht, The Netherlands
5
David H. Koch Center for Applied Research of Genitourinary Cancers, The University of Texas MD Anderson Cancer Center, Houston, TX 77230, USA
*
Author to whom correspondence should be addressed.
Cancers 2019, 11(10), 1459; https://doi.org/10.3390/cancers11101459
Received: 21 August 2019 / Revised: 24 September 2019 / Accepted: 26 September 2019 / Published: 29 September 2019
(This article belongs to the Special Issue Cancer Invasion and Metastasis)
Tumor metastasis is the endpoint of tumor progression and depends on the ability of tumor cells to locally invade tissue, transit through the bloodstream and ultimately to colonize secondary organs at distant sites. P120 catenin (p120) has been implicated as an important regulator of metastatic dissemination because of its roles in cell–cell junctional stability, cytoskeletal dynamics, growth and survival. However, conflicting roles for p120 in different tumor models and steps of metastasis have been reported, and the understanding of p120 functions is confounded by the differential expression of p120 isoforms, which differ in N-terminal length, tissue localization and, likely, function. Here, we used in silico exon expression analyses, in vitro invasion assays and both RT-PCR and immunofluorescence of human tumors. We show that alternative exon usage favors expression of short isoform p120-3 in 1098 breast tumors and correlates with poor prognosis. P120-3 is upregulated at the invasive front of breast cancer cells migrating as collective groups in vitro. Furthermore, we demonstrate in histological sections of 54 human breast cancer patients that p120-3 expression is maintained throughout the metastatic cascade, whereas p120-1 is differentially expressed and diminished during invasion and in metastases. These data suggest specific regulation and functions of p120-3 in breast cancer invasion and metastasis. View Full-Text
Keywords: adherens junctions; p120catenin; breast cancer adherens junctions; p120catenin; breast cancer
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Venhuizen, J.-H.; Span, P.N.; van den Dries, K.; Sommer, S.; Friedl, P.; Zegers, M.M. P120 Catenin Isoforms Differentially Associate with Breast Cancer Invasion and Metastasis. Cancers 2019, 11, 1459.

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