STAT3-Activated Long Non-Coding RNA Lung Cancer Associated Transcript 1 Drives Cell Proliferation, Migration, and Invasion in Hepatoblastoma Through Regulation of the miR-301b/STAT3 Axis

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 (<i>LUCAT1</i>) in HB. Analysis of data from The Cancer Genome Atlas indicated that upregulation of lncRNA <i>LUCAT1</i> was closely associated with poor overall survival of HB patients. Quantitative reverse transcription polymerase chain reaction analysis showed that <i>LUCAT1</i> was highly expressed in both HB tissues and cell lines. Loss-of function assays to identify the biological function of <i>LUCAT1</i> in HB showed that <i>LUCAT1</i> knockdown inhibited cell proliferation, migration, and invasion but reversed epithelial-mesenchymal transition. Luciferase assays indicated that <i>STAT3</i> was a transcription activator of <i>LUCAT1</i> and that <i>LUCAT1</i> could increase <i>STAT3</i> expression by competitively binding to <i>miR-301b</i>. In conclusion, it was found that <i>LUCAT1</i> was activated by <i>STAT3</i> and promoted cell proliferation, migration, and invasion in HB through modulation of the <i>miR-301b/STAT3</i> axis.