Oncotarget

Research Papers:

DcR3 induces epithelial-mesenchymal transition through activation of the TGF-β3/SMAD signaling pathway in CRC

Yan-Ping Liu, Hui-Fang Zhu, Ding-li Liu, Zhi-Yan Hu, Sheng-Nan Li, He-Ping Kan, Xiao-Yan Wang _ and Zu-Guo Li

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Oncotarget. 2016; 7:77306-77318. https://doi.org/10.18632/oncotarget.12639

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Abstract

Yan-Ping Liu1,2,3,*, Hui-Fang Zhu1,2,3,*, Ding-li Liu4,*, Zhi-Yan Hu1,2,3, Sheng-Nan Li1,2,3, He-Ping Kan5, Xiao-Yan Wang1,2,3, Zu-Guo Li1,2,3

1Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China

2Guangdong Provincial Key Laboratory of Molecular Tumour Pathology, Guangzhou, China

3Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China

4State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China

5Department of Hepatobiliary Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China

*These authors have contributed equally to this work

Correspondence to:

Xiao-Yan Wang, email: [email protected]

Zu-Guo Li, email: [email protected]

Keywords: decoy receptor 3, colorectal cancer, TGF-β3/SMAD signaling, metastasis, epithelial-mesenchymal transition

Received: May 30, 2016    Accepted: September 28, 2016    Published: October 13, 2016

ABSTRACT

Decoy receptor 3 (DcR3), a novel member of the tumor necrosis factor receptor (TNFR) family, was recently reported to be associated with tumorigenesis and metastasis. However, the role of DcR3 in human colorectal cancer (CRC) has not been fully elucidated. In this study, we found that DcR3 expression was significantly higher in human colorectal cancer tissues than in paired normal tissues, and that DcR3 expression was strongly correlated with tumor invasion, lymph node metastases and poor prognoses. Moreover, DcR3 overexpression significantly enhanced CRC cell proliferation and migration in vitro and tumorigenesis in vivo. Conversely, DcR3 knockdown significantly repressed CRC cell proliferation and migration in vitro, and DcR3 deficiency also attenuated CRC tumorigenesis and metastasis in vivo. Functionally, DcR3 was essential for TGF-β3/SMAD-mediated epithelial-mesenchymal transition (EMT) of CRC cells. Importantly, cooperation between DcR3 and TGF-β3/SMAD-EMT signaling-related protein expression was correlated with survival and survival time in CRC patients. In conclusion, our results demonstrate that DcR3 may be a prognostic biomarker for CRC and that this receptor facilitates CRC development and metastasis by participating in TGF-β3/SMAD-mediated EMT of CRC cells.


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