Table of Contents
Molecular Biology International
Volume 2012, Article ID 196715, 10 pages
Research Article

The SARAH Domain of RASSF1A and Its Tumor Suppressor Function

1AWG Tumor Genetics of the Medical Faculty, Martin-Luther-University Halle-Wittenberg, 06108 Halle, Germany
2OncoRay, National Center for Radiation Research in Oncology, Medical Faculty Carl Gustav Carus, University of Technology, 06108 Halle, Dresden, Germany
3Institute for Genetics, Justus-Liebig University Giessen, 35392 Giessen, Germany

Received 16 November 2011; Revised 1 February 2012; Accepted 2 February 2012

Academic Editor: Geoffrey J. Clark

Copyright © 2012 Claudia Dittfeld et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The Ras association domain family 1A (RASSF1A) tumor suppressor encodes a Sav-RASSF-Hpo domain (SARAH), which is an interaction domain characterized by hWW45 (dSAV) and MST1/2 (dHpo). In our study, the interaction between RASSF1A and RASSF1C with MST1 and MST2 was demonstrated and it was shown that this interaction depends on the SARAH domain. SARAH domain-deleted RASSF1A had a similar growth-reducing effect as full-length RASSF1A and inhibited anchorage independent growth of the lung cancer cell lines A549 significantly. In cancer cells expressing the SARAH deleted form of RASSF1A, reduced mitotic rates ( ) with abnormal metaphases ( ) were observed and a significantly increased rate of apoptosis was found ( ) compared to full-length RASSF1A. Although the association with microtubules and their stabilization was unaffected, mitotic spindle formation was altered by deletion of the SARAH domain of RASSF1A. In summary, our results suggest that the SARAH domain plays an important role in regulating the function of RASSF1A.