Hepatoblastoma (HB) usually occurs in infants and toddlers. Although long non-coding RNAs (lncRNAs) in various human cancers have been widely studied, the role of lncRNAs in HB remains unclear. This… Click to show full abstract
Hepatoblastoma (HB) usually occurs in infants and toddlers. Although long non-coding RNAs (lncRNAs) in various human cancers have been widely studied, the role of lncRNAs in HB remains unclear. This study aimed to investigate the biological role of the lncRNA lung cancer associated transcript 1 (LUCAT1) in HB. Analysis of data from The Cancer Genome Atlas indicated that upregulation of lncRNA LUCAT1 was closely associated with poor overall survival of HB patients. Quantitative reverse transcription polymerase chain reaction analysis showed that LUCAT1 was highly expressed in both HB tissues and cell lines. Loss-of function assays to identify the biological function of LUCAT1 in HB showed that LUCAT1 knockdown inhibited cell proliferation, migration, and invasion but reversed epithelial-mesenchymal transition. Luciferase assays indicated that STAT3 was a transcription activator of LUCAT1 and that LUCAT1 could increase STAT3 expression by competitively binding to miR-301b. In conclusion, it was found that LUCAT1 was activated by STAT3 and promoted cell proliferation, migration, and invasion in HB through modulation of the miR-301b/STAT3 axis.
               
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