Periostin attenuates tumor growth by inducing apoptosis in colitis-related colorectal cancer
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Yusuke Shimoyama1,3, Keiichi Tamai1, Rie Shibuya1, Mao Nakamura2, Mai Mochizuki1, Kazunori Yamaguchi2, Yoichi Kakuta3, Yoshitaka Kinouchi3, Ikuro Sato4, Akira Kudo5, Tooru Shimosegawa3 and Kennichi Satoh1
1Division of Cancer Stem Cell, Miyagi Cancer Center Research Institute, Natori, Japan
2Division of Molecular and Cellular Oncology, Miyagi Cancer Center Research Institute, Natori, Japan
3Department of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan
4Department of Pathology, Miyagi Cancer Center, Natori, Japan
5Department of Biological Information, Tokyo Institute of Technology, Yokohama, Japan
Keiichi Tamai, email: [email protected]
Keywords: periostin; colorectal cancer; colitis; apoptosis
Received: September 15, 2017 Accepted: March 17, 2018 Published: April 13, 2018
Inflammatory bowel diseases, which are multifactorial autoimmune colitis diseases, are occurring with increasing prevalence. One of the most serious complications of these diseases is colorectal cancer. Here we investigated the role of periostin (Postn), a matricellular protein that interacts with various integrin molecules on the cell surface, in colitis-induced colorectal cancer. Immunohistochemistry of mouse and human colorectal cancer samples revealed that Postn was expressed in the stroma and was upregulated in close proximity to the cancer cells. The colonic tumorigenesis in an inflammation-related colon carcinogenesis mouse model was increased in Postn knock-out (Postn−/−) mice compared to Postn+/+ mice. Although no difference was found in the degree of colitis between Postn+/+ and Postn−/− mice, Postn inhibited tumor growth and induced the apoptosis of mouse rectal cancer cells in vitro. Furthermore, fewer apoptotic colorectal cancer cells were observed in Postn−/− than in Postn+/+ mice. These data suggested that Postn has an anti-tumor effect on colitis-induced colorectal cancer.
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