Journal
CANCER BIOLOGY & THERAPY
Volume 7, Issue 8, Pages 1297-1301Publisher
LANDES BIOSCIENCE
DOI: 10.4161/cbt.7.8.6301
Keywords
c-jun; cancer; apoptosis; deoxyribozyme; liposarcoma; orthotopic; gene therapy
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Funding
- Australian Orthopaedics Association
- Victorian Orthopaedics Research Trust Grant
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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.
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