Format

Send to

Choose Destination
Cancer Cell. 2002 Aug;2(2):139-48.

Epigenetic changes in tumor Fas levels determine immune escape and response to therapy.

Author information

1
Department of Radiation Oncology, Stanford University Medical Center, CCSR South, 269 Campus Drive, Stanford, California 94305, USA. hmaecker@gene.com

Abstract

Epigenetic regulation of gene expression significantly influences cell growth and differentiation. Here we show that epigenetic silencing of Fas determines tumor growth in vivo and apoptotic sensitivity in vitro. In established tumors with epigenetically repressed Fas, restoration of Fas activity either by transfection of fas or treatment with Trichostatin A (TSA), an inhibitor of histone deacetylase, suppresses tumor growth and restores chemosensitivity. The TSA-dependent chemosensitivity and tumor growth control require both tumor Fas and the host NK (natural killer) cell functions. This work demonstrates the importance of epigenetic modification of Fas in tumor progression and immune evasion, and emphasizes the essential interplay between Fas and innate immunity in the control of chemoresistant tumors.

PMID:
12204534
DOI:
10.1016/s1535-6108(02)00095-8
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center