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http://purl.uniprot.org/citations/31300015http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31300015http://www.w3.org/2000/01/rdf-schema#comment"

Background

The mechanism underlying breast cancer stem cell (BCSCs) characteristics remains to be fully elucidated. Accumulating evidence implies that long noncoding RNAs (lncRNAs) play a pivotal role in regulating BCSCs stemness.

Methods

LncRNA LUCAT1 expression was assessed in breast cancer tissues (n = 151 cases) by in situ hybridization. Sphere-formation assay and colony formation assay were used to detect cell self-renewal and proliferation, respectively. RNA immunoprecipitation, RNA pull down and luciferase reporter assays were used to identify LUCAT1 and TCF7L2 as the direct target of miR-5582-3p. The activity of the Wnt/β-catenin pathway was analyzed by TOP/FOP-Flash reporter assays, western blot and immunohistochemistry (IHC).

Results

This study found LUCAT1 expression was related to tumor size (p = 0.015), lymph node metastasis (p = 0.002) and TNM staging (p < 0.001). High LUCAT1 expression indicated a shorter overall survival (p = 0.006) and disease-free survival (p = 0.011). Furthermore, LUCAT1 was more expressed in BCSCs than in breast cancer cells (BCCs) by lncRNA microarray chips. LUCAT1 up-regulation promoted proliferation of BCCs, while LUCAT1 down-regulation inhibited self-renewal of BCSCs. MiR-5582-3p was directly bound to LUCAT1 and TCF7L2 and negatively regulated their expression. LUCAT1 affected Wnt/β-catenin pathway.

Conclusions

LUCAT1 might be a significant biomarker to evaluate prognosis in breast cancer. LUCAT1 increased stem-like properties of BCCs and stemness of BCSCs by competitively binding miR-5582-3p with TCF7L2 and enhancing the Wnt/β-catenin pathway. The LUCAT1/miR-5582-3p/TCF7L2 axis provides insights for regulatory mechanism of stemness, and new strategies for clinical practice."xsd:string
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http://purl.uniprot.org/citations/31300015http://purl.uniprot.org/core/author"Mao X."xsd:string
http://purl.uniprot.org/citations/31300015http://purl.uniprot.org/core/author"Song X."xsd:string
http://purl.uniprot.org/citations/31300015http://purl.uniprot.org/core/author"Zhang L."xsd:string
http://purl.uniprot.org/citations/31300015http://purl.uniprot.org/core/author"Zhao L."xsd:string
http://purl.uniprot.org/citations/31300015http://purl.uniprot.org/core/author"Jin F."xsd:string
http://purl.uniprot.org/citations/31300015http://purl.uniprot.org/core/author"Zheng A."xsd:string
http://purl.uniprot.org/citations/31300015http://purl.uniprot.org/core/author"Wei M."xsd:string
http://purl.uniprot.org/citations/31300015http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31300015http://purl.uniprot.org/core/name"J Exp Clin Cancer Res"xsd:string
http://purl.uniprot.org/citations/31300015http://purl.uniprot.org/core/pages"305"xsd:string
http://purl.uniprot.org/citations/31300015http://purl.uniprot.org/core/title"Long non-coding RNA LUCAT1/miR-5582-3p/TCF7L2 axis regulates breast cancer stemness via Wnt/beta-catenin pathway."xsd:string
http://purl.uniprot.org/citations/31300015http://purl.uniprot.org/core/volume"38"xsd:string
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