RASSF1A-mediated mechanism controlling tumor dedifferentiation and aggressive oncogenic behavior

This study is a continuation of many previous research articles on lung cancer development that represented the first investigation target, from the initiation of our research group (MCG). Particularly, it shows that the RASSF1A tumor suppressor uncouples the NOTCH-HES1 axis by triggering SNURF/RNF4-mediated HES1 ubiquitination. Loss of RASSF1A promotes cancer stemness via NOTCH-independent HES1 stabilization and confers resistance to γ-secretase inhibitors (GSI). This is the first evidence of crosstalk between the Hippo and Notch pathways, through the RASSF1A tumor suppressor. The study provides insight into the clinical setting where the use of GSIs constitutes a productive therapeutic approach in oncology.

VG New

Prof. Vassilis G. Gorgoulis

Laboratory of Histology-Embryology
Molecular Carcinogenesis Group
Medical School
National and Kapodistrian University of Athens

 

Biomedical Research Foundation of the Academy of Athens

 

Faculty Institute for Cancer Sciences, University of Manchester,
Manchester Academic Health Science Centre, Manchester, UK

Manchester Centre for Cellular Metabolism,
University of Manchester, Manchester Academic Health Science Centre, Manchester

 

EMBO member

 

SenTraGorΤΜ

 

 

 

Office Tel: 0030 210-7462352
Fax: 0030 210-7462340
E-mail: vgorg@med.uoa.gr

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