Opisthorchis viverrini Infection Activates the PI3K/AKT/PTEN and Wnt/β-catenin Signaling Pathways in a Cholangiocarcinogenesis Model

Yothaisong, Supak; Thanee, Malinee; Namwat, Nisana; Yongvanit, Puangrat; Boonmars, Thidarut; Puapairoj, Anucha; Loilome, Watcharin

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자료유형: 학술저널

저자정보: Yothaisong, Supak (Department of Biochemistry, Faculty of Medicine, Khon Kaen University) Thanee, Malinee (Department of Biochemistry, Faculty of Medicine, Khon Kaen University) Namwat, Nisana (Department of Biochemistry, Faculty of Medicine, Khon Kaen University) Yongvanit, Puangrat (Department of Biochemistry, Faculty of Medicine, Khon Kaen University) Boonmars, Thidarut (Department of Parasitology, Faculty of Medicine, Khon Kaen University) Puapairoj, Anucha (Department of Pathology, Faculty of Medicine, Khon Kaen University) Loilome, Watcharin (Department of Biochemistry, Faculty of Medicine, Khon Kaen University)

저널정보: 아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제15권 제23호

발행연도: 2014.1

수록면: 10,463 - 10,468 (6page)

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Opisthorchis viverrini (Ov) infection is the major etiological factor for cholangiocarcinoma (CCA), especially in northeast Thailand. We have previously reported significant involvement of PI3K/AKT/PTEN and $Wnt/{\beta}$-catenin in human CCA tissues. The present study, therefore, examined the expression and activation of PI3K/AKT/PTEN and $Wnt/{\beta}$-catenin signaling components during Ov-induced cholangiocarcinogenesis in a hamster animal model. Hamsters were divided into two groups; non-treated and Ov plus NDMA treated. The results of immunohistochemical staining showed an upregulation of PI3K/AKT signaling as determined by elevated expression of the $p85{\alpha}$-regulatory and $p110{\alpha}$-catalytic subunits of PI3K as well as increased expression and activation of AKT during cholangiocarcinogenesis. Interestingly, the staining intensity of activated AKT (p-AKT) increased in the apical regions of the bile ducts and strong staining was detected where the liver fluke resides. Moreover, PTEN, a negative regulator of PI3K/AKT, was suppressed by decreased expression and increased phosphorylation during cholangiocarcinogenesis. We also detected upregulation of $Wnt/{\beta}$-catenin signaling as determined by increased positive staining of Wnt3, Wnt3a, Wnt5a, Wnt7b and ${\beta}$-catenin, corresponded with the period of cholangiocarcinogenesis. Furthermore, nuclear staining of ${\beta}$-catenin was observed in CCA tissues. Our results suggest the liver fluke infection causes chronic inflammatory conditions which lead to upregulation of the PI3K/AKT and $Wnt/{\beta}$-catenin signaling pathways which may drive CCA carcinogenesis. These results provide useful information for drug development, prevention and treatment of CCA.

#Opisthorchis viverrini #PI3K/AKT/PTEN #$Wnt/{beta}$-catenin #cholangiocarcinoma

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