| セッション情報 | Best Poster Award(Upper GI) |
|---|---|
| タイトル | IF-BP1-1 Pseudokinase Trib3 is Induced in Helicobacter pylori Infected Gastric Mucosa and Contributes to Gastric Carcinogenesis |
| 演者 | Yutaka Kondo（Division of GastroenterologyTohoku University Graduate School of MedicineJapan） |
| 共同演者 | Akira Imatani（Division of GastroenterologyTohoku University Graduate School of MedicineJapan）, Naoki Asano（Division of GastroenterologyTohoku University Graduate School of MedicineJapan）, Takashi Chiba（Division of GastroenterologyTohoku University Graduate School of MedicineJapan）, Jun Fushiya（Division of GastroenterologyTohoku University Graduate School of MedicineJapan）, Nobuyuki Ara（Division of GastroenterologyTohoku University Graduate School of MedicineJapan）, Kaname Uno（Division of GastroenterologyTohoku University Graduate School of MedicineJapan）, Yasuhiko Abe（Division of GastroenterologyTohoku University Graduate School of MedicineJapan）, Tomoyuki Koike（Division of GastroenterologyTohoku University Graduate School of MedicineJapan）, Katsunori Iijima（Division of GastroenterologyTohoku University Graduate School of MedicineJapan）, Tooru Shimosegawa（Division of GastroenterologyTohoku University Graduate School of MedicineJapan） |
| 抄録 | Helicobacter pylon’ （H． pyiori） infection is known to induce gastric intestinal metaplasia． This trans－differentiation is regarde d as the pre－cancerous state of gastric cancers and is characterized by the reduc－tion of Sox2 expression and the induction of Cdx2 expressionbut the details are still unclearTo rnimicthe process of gastric intestinal metaplasiawe established a normal mu血e gastric epitheHal cell linestably expressing Sox2－shRNA and aimed to identify the underlying factor related to gastric carcinogenersis downstream of down－regulated Sox2．Mi’croarray－based gene expression studies using these cells revealed that ／pseudokinase Tribbles homolog3 （ Trib3） was up－regulated by suppressing Sox2 expression． We then examined the effect of H．pylori in－fection on Trib3 expression． Quantitative real－time PCR and immunoblot analysis revealed that Trib3 is in－duced by H． pylori i nfection both in vitro and in vivoMoreover5’promoter reporter assay and im－rnunoblotting clarified that this induction was dependent on the activation of NF－i（B．Since Trib3 was expressed in gastric cancer cell lines and many of gastric caner tissueswe investigatedthe effect of Trib 3 expression on cell proliferation and colony formation． The proliferation and colonyforming capacity was significantly increased in Trib3 over￡xpressing cells in MTT assay and spheroidcolony assayrespectively． ln additionTrib3 over－expressing colony forming cells displayed increased ex－pression of cancer stem cell markers （CD44 and CD133）and this suggested that Trib3 is playing an im－portant role in gastric carcinogenesisIn conclusionour study suggested that H．pylori infection induces Trib3 via activation of NF－i〈B and sup－pression of Sox2and that Trib3 is involved in gastric carcinogenesis． |
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