| First Author | Yue C | Year | 2015 |
| Journal | Int J Cancer | Volume | 136 |
| Issue | 1 | Pages | 117-26 |
| PubMed ID | 24895110 | Mgi Jnum | J:289150 |
| Mgi Id | MGI:6430014 | Doi | 10.1002/ijc.29004 |
| Citation | Yue C, et al. (2015) Host STAT2/type I interferon axis controls tumor growth. Int J Cancer 136(1):117-26 |
| abstractText | The role of STAT2 in mediating the antigrowth effects of type I interferon (IFN) is well-documented in vitro. Yet evidence of IFN-activated STAT2 as having tumor suppressor function in vivo and participation in antitumor immunity is lacking. Here we show in a syngeneic tumor transplantation model that STAT2 reduces tumor growth. Stat2(-/-) mice formed larger tumors compared to wild type (WT) mice. IFN-beta treatment of Stat2(-/-) mice did not cause tumor regression. Gene expression analysis revealed a small subset of immunomodulatory genes to be downregulated in tumors established in Stat2(-/-) mice. Additionally, we found tumor antigen cross-presentation by Stat2(-/-) dendritic cells to T cells to be impaired. Adoptive transfer of tumor antigen specific CD8(+) T cells primed by Stat2(-/-) dendritic cells into tumor-bearing Stat2(-/-) mice did not induce tumor regression with IFN-beta intervention. We observed that an increase in the number of CD4(+) and CD8(+) T cells in the draining lymph nodes of IFN-beta-treated tumor-bearing WT mice was absent in IFN-beta treated Stat2(-/-) mice. Thus our study provides evidence for further evaluation of STAT2 function in cancer patients receiving type I IFN based immunotherapy. |
