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Exp Cell Res. 2018 Mar 1;364(1):59-67. doi: 10.1016/j.yexcr.2018.01.028. Epub 2018 Jan 31.

Silencing of Kangai 1 C-terminal interacting tetraspanin suppresses progression of cholangiocarcinoma.

Author information

1
Department of Internal Medicine I, Medical University Hospital, Tübingen, Germany; Department of Pathophysiology, Vietnam Military Medical University, Hanoi, Vietnam; Vietnamese-German Center for Medical Research, Hanoi, Vietnam; Institute of Tropical Medicine, Medical University Hospital, Tübingen, Germany.
2
Department of Internal Medicine I, Goethe University Hospital, Frankfurt, Germany.
3
Department of Gastroenterology, Shanghai Ruijin Hospital, Shanghai, China.
4
Department of Internal Medicine I, Medical University Hospital, Tübingen, Germany.
5
Department of Internal Medicine I, Medical University Hospital, Tübingen, Germany; Vietnamese-German Center for Medical Research, Hanoi, Vietnam; Institute of Tropical Medicine, Medical University Hospital, Tübingen, Germany.
6
Department of Pathophysiology, Vietnam Military Medical University, Hanoi, Vietnam; Vietnamese-German Center for Medical Research, Hanoi, Vietnam.
7
Vietnamese-German Center for Medical Research, Hanoi, Vietnam; 108 Military Central Hospital, Hanoi, Vietnam.
8
Vietnamese-German Center for Medical Research, Hanoi, Vietnam; Institute of Tropical Medicine, Medical University Hospital, Tübingen, Germany.
9
Institute of Pathology, Medical University Hospital, Tübingen, Germany.
10
Institute of Pathology, Hannover Regional Hospital, Hannover, Germany.
11
Department of Internal Medicine I, Medical University Hospital, Tübingen, Germany; Department of Internal Medicine II, Bremen-Nord Hospital, Bremen, Germany. Electronic address: ruben.plentz@klinikum-bremen-nord.de.

Abstract

Cholangiocarcinoma (CC) is the second most common primary hepatic malignancy. CC treatment options are very limited especially for patients with distant metastasis. Kangai 1 C-terminal interacting tetraspanin (KITENIN) is highly expressed in numerous cancers, but the role of KITENIN in CC remains unknown. Here, we have investigated for the first time the function of KITENIN in human CC cell lines (TFK-1, SZ-1), tissues and a CC mouse model (Alb-Cre/LSL-KRASG12D/p53L/L). KITENIN was expressed in 92.2% of human CC tissues, in murine CC samples and also in human CC cell lines. Knockdown of KITENIN by small interfering RNA (siRNA) effectively reduced proliferation, migration, invasion and colony formation in both intra- and extra-hepatic CC cells. The expression of epithelial-mesenchymal transition (EMT) markers like N-cadherin, Vimentin, Snail and Slug were suppressed in KITENIN knockdown CC cells. Our results indicate that KITENIN is crucial for cholangiocarcinogenesis and it might become a potential therapeutic target for human CC treatment.

KEYWORDS:

Cholangiocarcinoma; EMT; KITENIN

PMID:
29366806
DOI:
10.1016/j.yexcr.2018.01.028
[Indexed for MEDLINE]

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