| First Author | Yun HM | Year | 2015 |
| Journal | Oncotarget | Volume | 6 |
| Issue | 11 | Pages | 9061-72 |
| PubMed ID | 25909160 | Mgi Jnum | J:309321 |
| Mgi Id | MGI:6757318 | Doi | 10.18632/oncotarget.3197 |
| Citation | Yun HM, et al. (2015) IL-32alpha suppresses colorectal cancer development via TNFR1-mediated death signaling. Oncotarget 6(11):9061-72 |
| abstractText | Inflammation is associated with cancer-prone microenvironment, leading to cancer. IL-32 is expressed in chronic inflammation-linked human cancers. To investigate IL-32alpha in inflammation-linked colorectal carcinogenesis, we generated a strain of mice, expressing IL-32 (IL-32alpha-Tg). In IL-32alpha-Tg mice, azoxymethane (AOM)-induced colon cancer incidence was decreased, whereas expression of TNFR1 and TNFR1-mediated apoptosis was increased. Also, IL-32alpha increased ROS production to induce prolonged JNK activation. In colon cancer patients, IL-32alpha and TNFR1 were increased. These findings indicate that IL-32alpha suppressed colon cancer development by promoting the death signaling of TNFR1. |
