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Research Paper

Involvement of c-jun in human liposarcoma growth: supporting data from clinical immunohistochemistry and DNAzyme efficacy

Crispin R. Dass, Stuart J. Galloway, Jonathan C. M. Clark, Levon M. Khachigian and Peter F. M. Choong

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c-jun has been found to be upregulated in a variety of cancers. Recently, this oncogene has also been implicated in liposarcoma (LS) progression. c-jun knockdown mediated by a deoxyribozyme induced apoptosis in LS cells via evoking caspase-10, but not the Fas/FasL pathway. A novel orthotopic model for LS was established in the hindlimb of mice using human cells to extend the evaluation of effects of c-jun knockdown in vivo. Tumor take in vivo was 100%, with growths resembling high grade aggressive LS. The c-jun deoxyribozyme inhibited the growth of LS in this model. Clinically, downregulation of c-jun may proffer an improved treatment outcome for liposarcoma. The new model for LS described here will enable better testing of agents with therapeutic potential against LS.

Authors

Crispin R. Dass

Department of Orthopaedics and University of Melbourne Department of Surgery, St. Vincent's Hospital, VIC, Australia

Stuart J. Galloway

Department of Pathology, St. Vincent's Hospital, VIC, Australia

Jonathan C. M. Clark

Department of Orthopaedics and University of Melbourne Department of Surgery, St. Vincent's Hospital, VIC, Australia

Levon M. Khachigian

Centre for Vascular Research, UNSW and Prince of Wales Hospital, NSW, Australia

Peter F. M. Choong

Sarcoma Service, Peter MacCallum Cancer Institute, VIC, Australia/ Department of Orthopaedics and University of Melbourne Department of Surgery, St. Vincent's Hospital, VIC, Australia

Purchase article for $19

Subscribe to this journal for $129/year