Periostin attenuates tumor growth by inducing apoptosis in colitis-related colorectal cancer

// Yusuke Shimoyama 1, 3 , Keiichi Tamai 1 , Rie Shibuya 1 , Mao Nakamura 2 , Mai Mochizuki 1 , Kazunori Yamaguchi 2 , Yoichi Kakuta 3 , Yoshitaka Kinouchi 3 , Ikuro Sato 4 , Akira Kudo 5 , Tooru Shimosegawa 3 and Kennichi Satoh 1 1 Division of Cancer Stem Cell, Miyagi Cancer Center Research Institute, Natori, Japan 2 Division of Molecular and Cellular Oncology, Miyagi Cancer Center Research Institute, Natori, Japan 3 Department of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan 4 Department of Pathology, Miyagi Cancer Center, Natori, Japan 5 Department of Biological Information, Tokyo Institute of Technology, Yokohama, Japan Correspondence to: Keiichi Tamai, email: tamaikeiichi@med.tohoku.ac.jp Keywords: periostin; colorectal cancer; colitis; apoptosis Received: September 15, 2017      Accepted: March 17, 2018      Published: April 13, 2018 ABSTRACT 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.