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Cancer Research 67, 1090-1098, February 1, 2007. doi: 10.1158/0008-5472.CAN-06-3117
© 2007 American Association for Cancer Research
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Cell, Tumor, and Stem Cell Biology

The Type III Transforming Growth Factor-ß Receptor as a Novel Tumor Suppressor Gene in Prostate Cancer

Ryan S. Turley1, Elizabeth C. Finger2, Nadine Hempel2, Tam How2, Timothy A. Fields3 and Gerard C. Blobe1,2

Departments of 1 Medicine, 2 Pharmacology and Cancer Biology, and 3 Pathology, Duke University Medical Center, Durham, North Carolina

Requests for reprints: Gerard C. Blobe, 221B MSRB Research Drive, Box 2631, Duke University Medical Center, Durham, NC 27710. Phone: 919-668-1352; Fax: 919-668-2458; E-mail: blobe001{at}mc.duke.edu.

The transforming growth factor-ß (TGF-ß) signaling pathway has an important role in regulating normal prostate epithelium, inhibiting proliferation, differentiation, and both androgen deprivation–induced and androgen-independent apoptosis. During prostate cancer formation, most prostate cancer cells become resistant to these homeostatic effects of TGF-ß. Although the loss of expression of either the type I (TßRI) or type II (TßRII) TGF-ß receptor has been documented in ~30% of prostate cancers, most prostate cancers become TGF-ß resistant without mutation or deletion of TßRI, TßRII, or Smads2, 3, and 4, and thus, the mechanism of resistance remains to be defined. Here, we show that type III TGF-ß receptor (TßRIII or betaglycan) expression is decreased or lost in the majority of human prostate cancers as compared with benign prostate tissue at both the mRNA and protein level. Loss of TßRIII expression correlates with advancing tumor stage and a higher probability of prostate-specific antigen (PSA) recurrence, suggesting a role in prostate cancer progression. The loss of TßRIII expression is mediated by the loss of heterozygosity at the TGFBR3 genomic locus and epigenetic regulation of the TßRIII promoter. Functionally, restoring TßRIII expression in prostate cancer cells potently decreases cell motility and cell invasion through Matrigel in vitro and prostate tumorigenicity in vivo. Taken together, these studies define the loss of TßRIII expression as a common event in human prostate cancer and suggest that this loss is important for prostate cancer progression through effects on cell motility, invasiveness, and tumorigenicity. [Cancer Res 2007;67(3):1090–8]




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