| First Author | Zhang Q | Year | 2012 |
| Journal | Cancer Res | Volume | 72 |
| Issue | 10 | Pages | 2589-99 |
| PubMed ID | 22461511 | Mgi Jnum | J:189341 |
| Mgi Id | MGI:5445068 | Doi | 10.1158/0008-5472.CAN-11-3795 |
| Citation | Zhang Q, et al. (2012) Interleukin-17 promotes formation and growth of prostate adenocarcinoma in mouse models. Cancer Res 72(10):2589-99 |
| abstractText | The contributions of interleukin (IL)-17 to cancer remain unclear and somewhat controversial. We took a genetic approach to explore its role in prostate cancers by interbreeding IL-17 receptor C (IL-17RC)-deficient mice with mice that are conditionally mutant for PTEN, one established preclinical model for prostate cancer. Mice that were IL-17RC-deficient (IL-17RC(-)) displayed prostates that were smaller than mice that maintained IL-17RC expression (IL-17RC(+)). In addition, IL-17RC(-) mice developed a reduced number of invasive prostate adenocarcinomas with lower rates of cellular proliferation and higher apoptosis than IL-17RC(+) mice. Moreover, the fibromuscular stroma surrounding prostatic glands was relatively thicker in IL-17RC(-) mice and was associated with decreased matrix metalloproteinase (Mmp)7 expression and increased Timp1, 2, and 4 expression, whereas administration of recombinant mouse IL-17 induced prostatic expression of Mmp7. Taken together, our results suggested that IL-17 promotes the formation and growth of prostate adenocarcinoma, and that an IL-17-MMP7 signaling axis is required for the transition of prostatic intraepithelial neoplasia to frank adenocarcinoma. |
