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Loss of SM22 is a characteristic signature of colon carcinogenesis and its restoration suppresses colon tumorigenicity in vivo and in vitro
Author(s) -
Yeo Marie,
Park Hee Jin,
Kim DongKyu,
Kim Young Bae,
Cheong Jae Youn,
Lee Kwang Jae,
Cho Sung Won
Publication year - 2010
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/cncr.25003
Subject(s) - colorectal cancer , in vivo , carcinogenesis , cancer research , immunohistochemistry , cancer , adenocarcinoma , metastasis , medicine , pathology , western blot , biology , gene , biochemistry , microbiology and biotechnology
BACKGROUND: We previously found the down‐expression of SM22 in an experimental animal model of colorectal cancer by performing a proteomic analysis. In this study, we addressed the expression and molecular mechanisms of SM22 in human colorectal cancer. METHODS: To evaluate the expression of SM22 in colon cancers, Western blot and immunohistochemistry were performed in 13 normal, 14 adenomas, and 44 adenocarcinomas. To address the role of SM22 in colon carcinogenesis, SM22 was restored in the colon cancer cells by the transfection with the pIRES2 vector containing full‐length SM22 cDNA and tested for tumorigenicity in vivo and in vitro. RESULTS: SM22 was found to be significantly down‐regulated in adenocarcinoma (58%) compared with adenoma (21.4%) and normal (15.3%). The loss of SM22 correlated with poor differentiation of tumor ( P = 0.009) and lymph node metastasis ( P = 0.029). Restoration of SM22 expression inhibited cell migration, colony‐forming ability of cancer cells, and induced retardation of in vivo tumor growth in a xenograft model. CONCLUSIONS: Loss of SM22 is a molecular signature of colon cancer and is closely associated with progression, differentiation, and metastasis of colon cancer. The restoration of SM22 leads to an inhibition of colon carcinogenesis in vivo and in vitro, suggesting that SM22 might potentially function as a novel tumor suppressor. Cancer 2010. © 2010 American Cancer Society.