Up-regulation of lncRNA SNHG1 indicates poor prognosis and promotes cell proliferation and metastasis of colorectal cancer by activation of the Wnt/β-catenin signaling pathway
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Yuping Zhu1, Bo Li1, Zhuo Liu1, Lai Jiang1, Gang Wang1, Min Lv2 and Dechuan Li1
1Department of Colorectal Surgery, Zhejiang Cancer Hospital, Hangzhou 310022, Zhejiang Province, China
2Department of Ultrasonic, Zhejiang Cancer Hospital, Hangzhou 310022, Zhejiang Province, China
Dechuan Li, email: firstname.lastname@example.org
Keywords: colorectal cancer; SNHG1; Wnt/β-catenin; proliferation; metastasis
Received: June 19, 2017 Accepted: November 16, 2017 Published: December 04, 2017
Recently, the lncRNA small nucleolar RNA host gene (SNHG1) has been exhibited to be upregulated, which plays a crucial role in the development and prognosis of several cancers. However, the role of the biology and clinical significance of SNHG1 in the tumorigenesis of colorectal cancer (CRC) has rarely been reported. In this work, we firstly found that SNHG1 expression levels were upregulated aberrantly in colorectal cancer tissues and colorectal cancer cell lines. By Kaplan-Meier survival analysis, patients with high SNHG1 expression level had poorer overall survival (OS) and progression-free survival (PFS) than those with low SNHG1 expression. In multivariate analysis, increased SNHG1 expression was proved to be an independent unfavorable prognostic indicator for CRC. In vitro experiments revealed that SNHG1 silencing inhibited the growth and metastasis and induced apoptosis of CRC cell lines. Finally, we found that SNHG1 may induce the activation of the WNT/β-catenin pathway through regulating β-catenin expression and transcription factor-4 (TCF-4), cyclin D1 and MMP-9. Altogether, our findings demonstrated that lncRNA SNHG1, was high expressed in colorectal cancer tissues and may serve as a tumor oncogene through regulating WNT/β-catenin signal pathway, which provided a candidate diagnostic biomarker and a promising therapeutic target for patients with CRC.
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