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白细胞介素-32α通过肿瘤坏死因子受体1介导的死亡信号通路抑制结直肠癌的发展。

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

作者信息

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

机构信息

Department of Maxillofacial Tissue Regeneration, School of Dentistry and Research Center for Tooth & Periodontal Regeneration (MRC), Kyung Hee University, Seoul 130-701, Republic of Korea.

College of Pharmacy and Medical Research Center, Chungbuk National University, Heungduk-gu, Cheongju, Chungbuk 361-763, Republic of Korea.

出版信息

Oncotarget. 2015 Apr 20;6(11):9061-72. doi: 10.18632/oncotarget.3197.

DOI:10.18632/oncotarget.3197
PMID:25909160
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4496202/
Abstract

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.

摘要

炎症与易于引发癌症的微环境相关，进而导致癌症。白细胞介素-32（IL-32）在与慢性炎症相关的人类癌症中表达。为了研究IL-32α在与炎症相关的结直肠癌发生过程中的作用，我们培育了一种表达IL-32（IL-32α转基因）的小鼠品系。在IL-32α转基因小鼠中，偶氮甲烷（AOM）诱导的结肠癌发病率降低，而肿瘤坏死因子受体1（TNFR1）的表达及TNFR1介导的细胞凋亡增加。此外，IL-32α增加活性氧（ROS）的产生，以诱导JNK的持续激活。在结肠癌患者中，IL-32α和TNFR1水平升高。这些发现表明，IL-32α通过促进TNFR1的死亡信号传导来抑制结肠癌的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee0/4496202/da2077a8338a/oncotarget-06-9061-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee0/4496202/823ab41b9379/oncotarget-06-9061-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee0/4496202/c08d8ae3a6d1/oncotarget-06-9061-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee0/4496202/84778f19ce5c/oncotarget-06-9061-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee0/4496202/16e067520648/oncotarget-06-9061-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee0/4496202/4895aff9add2/oncotarget-06-9061-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee0/4496202/da2077a8338a/oncotarget-06-9061-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee0/4496202/823ab41b9379/oncotarget-06-9061-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee0/4496202/c08d8ae3a6d1/oncotarget-06-9061-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee0/4496202/84778f19ce5c/oncotarget-06-9061-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee0/4496202/16e067520648/oncotarget-06-9061-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee0/4496202/4895aff9add2/oncotarget-06-9061-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee0/4496202/da2077a8338a/oncotarget-06-9061-g006.jpg

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