S100A11 is required for efficient plasma membrane repair and survival of invasive cancer cells

Jyoti K. Jaiswal (), Stine P. Lauritzen, Luana Scheffer, Masakiyo Sakaguchi, Jakob Bunkenborg, Sanford M. Simon, Tuula Kallunki, Marja Jäättelä and Jesper Nylandsted ()
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Jyoti K. Jaiswal: Children’s National Medical Center, Center for Genetic Medicine Research
Stine P. Lauritzen: Unit for Cell Death and Metabolism, Danish Cancer Society Research Center
Luana Scheffer: Children’s National Medical Center, Center for Genetic Medicine Research
Masakiyo Sakaguchi: Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kitaku
Jakob Bunkenborg: Copenhagen University Hospital Hvidovre
Sanford M. Simon: Laboratory of Cellular Biophysics, The Rockefeller University
Tuula Kallunki: Unit for Cell Death and Metabolism, Danish Cancer Society Research Center
Marja Jäättelä: Unit for Cell Death and Metabolism, Danish Cancer Society Research Center
Jesper Nylandsted: Unit for Cell Death and Metabolism, Danish Cancer Society Research Center

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract Cell migration and invasion require increased plasma membrane dynamics and ability to navigate through dense stroma, thereby exposing plasma membrane to tremendous physical stress. Yet, it is largely unknown how metastatic cancer cells acquire an ability to cope with such stress. Here we show that S100A11, a calcium-binding protein upregulated in a variety of metastatic cancers, is essential for efficient plasma membrane repair and survival of highly motile cancer cells. Plasma membrane injury-induced entry of calcium into the cell triggers recruitment of S100A11 and Annexin A2 to the site of injury. We show that S100A11 in a complex with Annexin A2 helps reseal the plasma membrane by facilitating polymerization of cortical F-actin and excision of the damaged part of the plasma membrane. These data reveal plasma membrane repair in general and S100A11 and Annexin A2 in particular as new targets for the therapy of metastatic cancers.

Date: 2014
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DOI: 10.1038/ncomms4795

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