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Upregulation of musashi1 increases malignancy of hepatocellular carcinoma via the Wnt/β-catenin signaling pathway and predicts a poor prognosis

BACKGROUND: Hepatocellular carcinoma (HCC) is a common human malignant cancer due to a high metastatic capacity and the recurrence rate is also high. This study is aim to investigate the role of musashi1 as a potential biomarker for therapy of HCC. METHODS: The mRNA and protein expression levels of...

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Autores principales: Liu, Qiuhua, Zhou, Cuijie, Zhang, Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6937928/
https://www.ncbi.nlm.nih.gov/pubmed/31888604
http://dx.doi.org/10.1186/s12876-019-1150-6
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author Liu, Qiuhua
Zhou, Cuijie
Zhang, Bo
author_facet Liu, Qiuhua
Zhou, Cuijie
Zhang, Bo
author_sort Liu, Qiuhua
collection PubMed
description BACKGROUND: Hepatocellular carcinoma (HCC) is a common human malignant cancer due to a high metastatic capacity and the recurrence rate is also high. This study is aim to investigate the role of musashi1 as a potential biomarker for therapy of HCC. METHODS: The mRNA and protein expression levels of musashi1 were detected in HCC samples and cell lines. The malignant properties of HCC cells, including proliferation, invasion and migration were measured by overexpressing or knocking down expression of musashi1. Additionally, the correlation between musashi1 and clinicopathological indexes and prognosis were analyzed. The expression of CD44 was measured and the correlation between CD44 and musashi1 was analyzed. RESULTS: In vitro cytological experiments demonstrated that musashi1 was elevated in HCC samples and cell lines and this increased expression affected cancer cell viability, migration and invasive capacity by activating of the Wnt/β-catenin signaling pathway. Analysis of clinicopathological characteristics suggested that up-regulation of musashi1 was related to metastasis potential and a poor prognosis. Besides, there was a positive correlation between CD44 and musashi1 expression. Upregulation of musashi1 in malignant liver tumors may have contributed to the maintenance of stem-cell like characteristics of HCC cells. CONCLUSIONS: Upregulation of musashi1 could enhance malignant development of HCC cells and thus might be a novel marker for HCC therapy.
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spelling pubmed-69379282019-12-31 Upregulation of musashi1 increases malignancy of hepatocellular carcinoma via the Wnt/β-catenin signaling pathway and predicts a poor prognosis Liu, Qiuhua Zhou, Cuijie Zhang, Bo BMC Gastroenterol Research Article BACKGROUND: Hepatocellular carcinoma (HCC) is a common human malignant cancer due to a high metastatic capacity and the recurrence rate is also high. This study is aim to investigate the role of musashi1 as a potential biomarker for therapy of HCC. METHODS: The mRNA and protein expression levels of musashi1 were detected in HCC samples and cell lines. The malignant properties of HCC cells, including proliferation, invasion and migration were measured by overexpressing or knocking down expression of musashi1. Additionally, the correlation between musashi1 and clinicopathological indexes and prognosis were analyzed. The expression of CD44 was measured and the correlation between CD44 and musashi1 was analyzed. RESULTS: In vitro cytological experiments demonstrated that musashi1 was elevated in HCC samples and cell lines and this increased expression affected cancer cell viability, migration and invasive capacity by activating of the Wnt/β-catenin signaling pathway. Analysis of clinicopathological characteristics suggested that up-regulation of musashi1 was related to metastasis potential and a poor prognosis. Besides, there was a positive correlation between CD44 and musashi1 expression. Upregulation of musashi1 in malignant liver tumors may have contributed to the maintenance of stem-cell like characteristics of HCC cells. CONCLUSIONS: Upregulation of musashi1 could enhance malignant development of HCC cells and thus might be a novel marker for HCC therapy. BioMed Central 2019-12-30 /pmc/articles/PMC6937928/ /pubmed/31888604 http://dx.doi.org/10.1186/s12876-019-1150-6 Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Liu, Qiuhua
Zhou, Cuijie
Zhang, Bo
Upregulation of musashi1 increases malignancy of hepatocellular carcinoma via the Wnt/β-catenin signaling pathway and predicts a poor prognosis
title Upregulation of musashi1 increases malignancy of hepatocellular carcinoma via the Wnt/β-catenin signaling pathway and predicts a poor prognosis
title_full Upregulation of musashi1 increases malignancy of hepatocellular carcinoma via the Wnt/β-catenin signaling pathway and predicts a poor prognosis
title_fullStr Upregulation of musashi1 increases malignancy of hepatocellular carcinoma via the Wnt/β-catenin signaling pathway and predicts a poor prognosis
title_full_unstemmed Upregulation of musashi1 increases malignancy of hepatocellular carcinoma via the Wnt/β-catenin signaling pathway and predicts a poor prognosis
title_short Upregulation of musashi1 increases malignancy of hepatocellular carcinoma via the Wnt/β-catenin signaling pathway and predicts a poor prognosis
title_sort upregulation of musashi1 increases malignancy of hepatocellular carcinoma via the wnt/β-catenin signaling pathway and predicts a poor prognosis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6937928/
https://www.ncbi.nlm.nih.gov/pubmed/31888604
http://dx.doi.org/10.1186/s12876-019-1150-6
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