IL-32α suppresses colorectal cancer development via TNFR1-mediated death signaling

نویسندگان

  • Hyung-Mun Yun
  • Kyung-Ran Park
  • Eun-Cheol Kim
  • Sang Bae Han
  • Do Young Yoon
  • Jin Tae Hong
چکیده

Inflammation is associated with cancer-prone microenvironment, leading to cancer. IL-32 is expressed in chronic inflammation-linked human cancers. To investigate IL-32α in inflammation-linked colorectal carcinogenesis, we generated a strain of mice, expressing IL-32 (IL-32α-Tg). In IL-32α-Tg mice, azoxymethane (AOM)-induced colon cancer incidence was decreased, whereas expression of TNFR1 and TNFR1-mediated apoptosis was increased. Also, IL-32α increased ROS production to induce prolonged JNK activation. In colon cancer patients, IL-32α and TNFR1 were increased. These findings indicate that IL-32α suppressed colon cancer development by promoting the death signaling of TNFR1.

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عنوان ژورنال:

دوره 6  شماره 

صفحات  -

تاریخ انتشار 2015