当前位置: X-MOL 学术BMC Gastroenterol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Upregulation of musashi1 increases malignancy of hepatocellular carcinoma via the Wnt/β-catenin signaling pathway and predicts a poor prognosis.
BMC Gastroenterology ( IF 2.5 ) Pub Date : 2019-12-30 , DOI: 10.1186/s12876-019-1150-6
Qiuhua Liu 1 , Cuijie Zhou 1 , Bo Zhang 1
Affiliation  

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.

中文翻译:

musashi1的上调通过Wnt /β-catenin信号通路增加肝细胞癌的恶性程度,并预示不良预后。

背景技术肝细胞癌(HCC)由于转移能力强,是一种常见的人类恶性肿瘤,其复发率也很高。这项研究旨在调查musashi1作为治疗HCC的潜在生物标记物的作用。方法检测肝癌标本和细胞株中musashi1的mRNA和蛋白表达水平。HCC细胞的恶性特性,包括增殖,侵袭和迁移,是通过过表达或敲除musashi1的表达来测量的。此外,分析了musashi1与临床病理指标和预后之间的相关性。检测CD44的表达,分析CD44与musashi1的相关性。结果体外细胞学实验表明,musashi1在HCC样品和细胞系中升高,而这种增加的表达通过激活Wnt /β-catenin信号传导途径影响癌细胞的活力,迁移和侵袭能力。临床病理特征分析表明,musashi1的上调与转移潜力和不良预后有关。此外,CD44和musashi1表达之间存在正相关。musashi1在恶性肝肿瘤中的上调可能有助于维持HCC细胞的干细胞样特性。结论musashi1的上调可增强HCC细胞的恶性发展,因此可能是HCC治疗的新标志物。Wnt /β-catenin信号通路的激活引起的迁移和侵袭能力。临床病理特征分析表明,musashi1的上调与转移潜力和不良预后有关。此外,CD44和musashi1表达之间存在正相关。musashi1在恶性肝肿瘤中的上调可能有助于维持HCC细胞的干细胞样特性。结论musashi1的上调可增强HCC细胞的恶性发展,因此可能是HCC治疗的新标志物。Wnt /β-catenin信号通路的激活引起的迁移和侵袭能力。临床病理特征分析表明,musashi1的上调与转移潜力和不良预后有关。此外,CD44和musashi1表达之间存在正相关。musashi1在恶性肝肿瘤中的上调可能有助于维持HCC细胞的干细胞样特性。结论musashi1的上调可增强HCC细胞的恶性发展,因此可能是HCC治疗的新标志物。musashi1在恶性肝肿瘤中的上调可能有助于维持HCC细胞的干细胞样特性。结论musashi1的上调可增强HCC细胞的恶性发展,因此可能是HCC治疗的新标志物。musashi1在恶性肝肿瘤中的上调可能有助于维持HCC细胞的干细胞样特性。结论musashi1的上调可增强HCC细胞的恶性发展,因此可能是HCC治疗的新标志物。
更新日期:2019-12-30
down
wechat
bug