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

被引：30
|
作者：
Yun, Hyung-Mun [1 ,2 ]
Park, Kyung-Ran [1 ,2 ]
Kim, Eun-Cheol [1 ,2 ]
Han, Sang Bae [3 ,4 ]
Yoon, Do Young [5 ]
Hong, Jin Tae [3 ,4 ]
机构：
[1] Kyung Hee Univ, Dept Maxillofacial Tissue Regenerat, Sch Dent, Seoul 130701, South Korea
[2] Kyung Hee Univ, Res Ctr Tooth & Periodontal Regenerat MRC, Seoul 130701, South Korea
[3] Chungbuk Natl Univ, Coll Pharm, Cheongju 361763, Chungbuk, South Korea
[4] Chungbuk Natl Univ, Med Res Ctr, Cheongju 361763, Chungbuk, South Korea
[5] Konkuk Univ, Dept Biosci & Biotechnol, Bio Mol Informat Ctr, Seoul 150716, South Korea
来源：
ONCOTARGET | 2015年 / 6卷 / 11期
基金：
新加坡国家研究基金会;
关键词：
IL-32; alpha; colon cancer; TNFR1; RIP1; NF-KAPPA-B; NECROSIS-FACTOR RECEPTOR; INFLAMMATORY-BOWEL-DISEASE; REACTIVE OXYGEN; TNF; ACTIVATION; INTERLEUKIN-32; INACTIVATION; APOPTOSIS; RISK;
D O I：
10.18632/oncotarget.3197
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Inflammation is associated with cancer-prone microenvironment, leading to cancer. IL-32 is expressed in chronic inflammation-linked human cancers. To investigate IL-32 alpha in inflammation-linked colorectal carcinogenesis, we generated a strain of mice, expressing IL-32 (IL-32 alpha-Tg). In IL-32 alpha-Tg mice, azoxymethane (AOM)-induced colon cancer incidence was decreased, whereas expression of TNFR1 and TNFR1-medicated apoptosis was increased. Also, IL-32 alpha increased ROS production to induce prolonged JNK activation. In colon cancer patients, IL-32 alpha and TNFR1 were increased. These findings indicate that IL-32 alpha suppressed colon cancer development by promoting the death signaling of TNFR1.
引用
收藏
页码：9061 / 9072
页数：12
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