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Aquaporin-1 in breast cancer

Traberg-Nyborg, Laura ; Login, Frédéric H. ; Edamana, Sarannya ; Tramm, Trine ; Borgquist, Signe LU and Nejsum, Lene N. (2022) In APMIS 130(1). p.3-10
Abstract

The canonical function of aquaporin (AQP) water channels is to facilitate passive transport of water across cellular membranes making them essential in the regulation of body water homeostasis. Moreover, AQPs, including AQP1, have been found to be overexpressed in multiple cancer types, including breast cancer, where AQP1 overexpression is associated with poor prognosis. AQPs have been shown to affect cellular processes associated with cancer progression and spread including cell migration, angiogenesis, and proliferation. Moreover, AQPs can regulate levels of adhesion proteins at cell–cell junctions, a regulatory role, which is still largely unexplored in cancer. Understanding the molecular mechanisms of how AQP1 contributes to breast... (More)

The canonical function of aquaporin (AQP) water channels is to facilitate passive transport of water across cellular membranes making them essential in the regulation of body water homeostasis. Moreover, AQPs, including AQP1, have been found to be overexpressed in multiple cancer types, including breast cancer, where AQP1 overexpression is associated with poor prognosis. AQPs have been shown to affect cellular processes associated with cancer progression and spread including cell migration, angiogenesis, and proliferation. Moreover, AQPs can regulate levels of adhesion proteins at cell–cell junctions, a regulatory role, which is still largely unexplored in cancer. Understanding the molecular mechanisms of how AQP1 contributes to breast cancer progression and metastatic processes is essential to establish AQP1 as a biomarker and to develop targeted anticancer treatments for breast cancer patients. This mini-review focuses on the role of AQP1 in breast cancer.

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author
; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
aquaporin-1, biomarker, Breast cancer, cancer progression, carcinomas
in
APMIS
volume
130
issue
1
pages
3 - 10
publisher
John Wiley & Sons Inc.
external identifiers
  • scopus:85119659451
  • pmid:34758159
ISSN
0903-4641
DOI
10.1111/apm.13192
language
English
LU publication?
yes
id
1695e029-d74d-4f0e-8c25-1757b4ddfd19
date added to LUP
2021-12-10 12:23:27
date last changed
2024-06-17 01:09:56
@article{1695e029-d74d-4f0e-8c25-1757b4ddfd19,
  abstract     = {{<p>The canonical function of aquaporin (AQP) water channels is to facilitate passive transport of water across cellular membranes making them essential in the regulation of body water homeostasis. Moreover, AQPs, including AQP1, have been found to be overexpressed in multiple cancer types, including breast cancer, where AQP1 overexpression is associated with poor prognosis. AQPs have been shown to affect cellular processes associated with cancer progression and spread including cell migration, angiogenesis, and proliferation. Moreover, AQPs can regulate levels of adhesion proteins at cell–cell junctions, a regulatory role, which is still largely unexplored in cancer. Understanding the molecular mechanisms of how AQP1 contributes to breast cancer progression and metastatic processes is essential to establish AQP1 as a biomarker and to develop targeted anticancer treatments for breast cancer patients. This mini-review focuses on the role of AQP1 in breast cancer.</p>}},
  author       = {{Traberg-Nyborg, Laura and Login, Frédéric H. and Edamana, Sarannya and Tramm, Trine and Borgquist, Signe and Nejsum, Lene N.}},
  issn         = {{0903-4641}},
  keywords     = {{aquaporin-1; biomarker; Breast cancer; cancer progression; carcinomas}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{3--10}},
  publisher    = {{John Wiley & Sons Inc.}},
  series       = {{APMIS}},
  title        = {{Aquaporin-1 in breast cancer}},
  url          = {{http://dx.doi.org/10.1111/apm.13192}},
  doi          = {{10.1111/apm.13192}},
  volume       = {{130}},
  year         = {{2022}},
}