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Published on: June 13, 2019
Involvement of c-jun in human liposarcoma growth: supporting data from clinical immunohistochemistry and DNAzyme
Crispin R Dass1, Stuart J Galloway, Jonathan C M Clark
1Department of Orthopaedics and University of Melbourne Department of Surgery, St. Vincent's Hospital, Fitzroy, Victoria, Australia. cris.dass@yahoo.com
Abstract:
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.
