Immunohistochemical evalulation of activated Ras and Rac1 as potential downstream effectors of aquaporin-5 in breast cancer in vivo

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  • Helene H Jensen
  • ,
  • Frédéric H Login
  • Ji-Young Park, Department of Pathology, School of Medicine, Kyungpook National University, Taegu, 41944, South Korea.
  • ,
  • Tae-Hwan Kwon, Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Taegu, 41944, South Korea. Electronic address: thkwon@knu.ac.kr.
  • ,
  • Lene N Nejsum

Aberrant levels of aquaporin-5 (AQP5) expression have been observed in several types of cancer, including breast cancer, where AQP5 overexpression is associated with metastasis and poor prognosis. In cultured cancer cells, AQP5 facilitates cell migration and activates Ras signaling. Both increased cell migration and Ras activation are associated with cancer metastasis, but so far it is unknown if AQP5 also affects these processes in vivo. Therefore, we investigated if high AQP5 expression in breast cancer tissue correlated with increased activation of Ras and of Rac1, which is a GTPase also involved in cell migration. This was accomplished by immunohistochemical analysis of invasive ductal carcinoma of breast tissue sections from human patients, followed by qualitative and quantitative correlation analysis between AQP5 and activated Ras and Rac1. Immunohistochemistry revealed that activation of Ras and Rac1 was positively correlated. There was, however, no correlation between high AQP5 expression and activation of Ras, whereas a nonsignificant, but positive, tendency between the levels of AQP5 and activated Rac1 levels was observed. In summary, this is the first report that correlates AQP5 expression levels to downstream signaling partners in breast cancer tissue sections. The results suggest Rac1 as a potential downstream signaling partner of AQP5 in vivo.

OriginalsprogEngelsk
TidsskriftBiochemical and Biophysical Research Communications
Vol/bind493
Nummer3
Sider (fra-til)1210-1216
Antal sider7
ISSN0006-291X
DOI
StatusUdgivet - 25 nov. 2017

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