| セッション情報 |
The 2nd JSGE International Topic Conference Poster Session
Colitis-Associated Cancer
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| タイトル |
IT-P-13：Serine Protease Inhibitor Kazal Type 1 Promote a Carcinogenesis of the Colon
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| 演者 |
Ida Satoshi（Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Japan） |
| 共同演者 |
Miyamoto Yuji（Department of Gastroenterological Surgery, Kumamoto University, Japan）, Watanabe Masayuki（Department of Gastroenterological Surgery, Kumamoto University, Japan）, Baba Hideo（Department of Gastroenterological Surgery, Kumamoto University, Japan）, Maehara Yoshihiko（Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Japan） |
| 抄録 |
＜Backgrounds and Aim＞Colitis-associated cancer（CAC）is the most serious complication of inflammatory bowel disease（IBD）.However, the pathogenesis of CAC is still uncertain. Serine protease inhibitor Kazal type 1（SPINK1：mouse homolog Spink3）is mainly produced in the pancreatic acinar cells. However, SPINK1 is expressed in various cancers and inflammatory state, including colon cancer and IBD. Interestingly, there are structural similarities between SPINK1 and epidermal growth factor（EGF）. Hence, we hypothesized that SPINK1 plays a role as the growth factor for tissue repair in the inflammatory state, and if prolonged, it works to carcinogenesis in the colon tissue. ＜Methods＞1）Proliferation of colon cancer cell lines examined in silencing and overexpression of SPINK1. 2）We used an efficient animal model for CAC carcinogenesis. Male C57BL/6 mice were given a single intraperitoneal administration of azoxymethane（AOM）, followed by a 1-week oral exposure to dextran sodium sulfate（DSS）. ＜Results＞1）SPINK1 induced proliferation of colon cancer cell lines. 2）Expression of Spink3 was observed in colitis induced by DSS. Furthermore, Spink3 were overexpressed in the cancerous tissues. Next, the tumor number of SPINK1 overexpression transgenic mice was significantly increased. ＜Conclusion＞SPINK1 was a critical tumor promoter during CAC progression. Furthermore, SPINK1 may work through EGFR, extensive further studies are necessary to develop a new target of prevention of CAC. |
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