Aquaporin-5 regulation of cell–cell adhesion proteins: an elusive “tail” story

American Journal of Physiology - Cell Physiology - Tập 320 Số 3 - Trang C282-C292 - 2021
Frédéric H. Login1, Johan Palmfeldt1, Joleen S. Cheah2, Soichiro Yamada2, Lene N. Nejsum1
1Department of Clinical Medicine, Aarhus University, Aarhus, Denmark
2Department of Biomedical Engineering, University of California, Davis, California

Tóm tắt

Aquaporins (AQPs) are water channels that facilitate transport of water across cellular membranes. AQPs are overexpressed in several cancers. Especially in breast cancer, AQP5 overexpression correlates with spread to lymph nodes and poor prognosis. Previously, we showed that AQP5 expression reduced cell–cell adhesion by reducing levels of adherens and tight-junction proteins (e.g., ZO-1, plakoglobin, and β-catenin) at the actual junctions. Here, we show that, when targeted to the plasma membrane, the AQP5 COOH-terminal tail domain regulated junctional proteins and, moreover, that AQP5 interacted with ZO-1, plakoglobin, β-catenin, and desmoglein-2, which were all reduced at junctions upon AQP5 overexpression. Thus, our data suggest that AQP5 mediates the effect on cell–cell adhesion via interactions with junctional proteins independently of AQP5-mediated water transport. AQP5 overexpression in cancers may thus contribute to carcinogenesis and cancer spread by two independent mechanisms: reduced cell–cell adhesion, a characteristic of epithelial-mesenchymal transition, and increased cell migration capacity via water transport.

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American Journal of Physiology - Cell Physiology

Tập 320 Số 3

C282-C292

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