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LRP16 prevents hepatocellular carcinoma progression through regulation of Wnt/β-catenin signaling

LRP16 prevents hepatocellular carcinoma progression through regulation of Wnt/β-catenin signaling Elevated LRP16expressionisassociatedwithpoorclinical outcomes in multiple malignancies. We detected LRP16 expression in hepatocellular carcinoma (HCC) and found that it was downregulated in tumor samples and HCC cell lines. In a cohort of 80 HCC patients, high level of LRP16 expression in HCC tumors was associated with well differentiation, less lymph node metastasis, and good overall survival (OS). Overexpression of LRP16 in the HepG2 and MHCC-97L cell lines increased cell apoptosis, attenuated cell proliferation, migration, and invasion ability in vitro, and drastically diminished tumor growth and metastasis in vivo. Silencing LRP16 in HCC-LM3 and SMMC-7721 cell lines showed opposite results. Microarray evaluation of tumor cells overexpressing LRP16 revealed the effects on decreased activity in the Wnt signaling pathway. These results were confirmed by qRT-PCR and Western blots. Furthermore, inhibition of Wnt signaling decreased proliferation, migration, and invasion of HCC cell lines. Mechanism conducted showed that LRP16 overexpression could prevent β-catenin from entering the nucleus. Our study demonstrated that LRP16 suppresses tumor growth in HCC by modulating Wnt/β-catenin signaling. Key messages & LRP16 was low expression in HCC tissue and cell lines. & Low expression of LRP16 in HCC was associated with poor prognosis. & LRP16 inhibits activation of the Wnt/β-catenin pathway http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Molecular Medicine Springer Journals

LRP16 prevents hepatocellular carcinoma progression through regulation of Wnt/β-catenin signaling

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Publisher
Springer Journals
Copyright
Copyright © 2018 by Springer-Verlag GmbH Germany, part of Springer Nature
Subject
Biomedicine; Molecular Medicine; Human Genetics; Internal Medicine
ISSN
0946-2716
eISSN
1432-1440
DOI
10.1007/s00109-018-1639-4
Publisher site
See Article on Publisher Site

Abstract

Elevated LRP16expressionisassociatedwithpoorclinical outcomes in multiple malignancies. We detected LRP16 expression in hepatocellular carcinoma (HCC) and found that it was downregulated in tumor samples and HCC cell lines. In a cohort of 80 HCC patients, high level of LRP16 expression in HCC tumors was associated with well differentiation, less lymph node metastasis, and good overall survival (OS). Overexpression of LRP16 in the HepG2 and MHCC-97L cell lines increased cell apoptosis, attenuated cell proliferation, migration, and invasion ability in vitro, and drastically diminished tumor growth and metastasis in vivo. Silencing LRP16 in HCC-LM3 and SMMC-7721 cell lines showed opposite results. Microarray evaluation of tumor cells overexpressing LRP16 revealed the effects on decreased activity in the Wnt signaling pathway. These results were confirmed by qRT-PCR and Western blots. Furthermore, inhibition of Wnt signaling decreased proliferation, migration, and invasion of HCC cell lines. Mechanism conducted showed that LRP16 overexpression could prevent β-catenin from entering the nucleus. Our study demonstrated that LRP16 suppresses tumor growth in HCC by modulating Wnt/β-catenin signaling. Key messages & LRP16 was low expression in HCC tissue and cell lines. & Low expression of LRP16 in HCC was associated with poor prognosis. & LRP16 inhibits activation of the Wnt/β-catenin pathway

Journal

Journal of Molecular Medicine – Springer Journals

Published: May 11, 2018

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