Background: Long noncoding RNA (LncRNA) UCA1 has been reported to function as an oncogene in multiple cancers. However, the biological roles and underlying mechanism of UCA1 in papillary thyroid carcinoma (PTC) remain unclear. This study aimed to investigate the underlying function of UCA1 on thyroid cancer progression.
Materials and methods: A series of experiments involving Cell Counting Kit-8, wound-healing, and transwell invasion assays were conducted to determine the cellular capabilities of proliferation, migration, and invasion, respectively. Binding sites between UCA1 and miR-204 were identified using a luciferase reporter system, whereas mRNA and protein expression of target genes were determined by real-time quantitative reverse transcription-PCR (qRT-PCR) and Western blot, respectively.
Results: The results revealed that UCA1 was upregulated in PTC tissue and cell lines. UCA1 knockdown significantly suppressed the cell proliferation, migration, and invasion of TPC-1 cells. Bioinformatics analysis and luciferase reporter assay verified the complementary binding within UCA1 and miR-204 at the 3'-UTR. Moreover, miR-204 inhibition reversed the UCA1 knockdown-mediated inhibitory effect on cell proliferation, migration, and invasion. We also found that UCA1 could regulate expression of IGFBP5, a direct target of miR-204 in PTC.
Conclusion: Our study demonstrated that UCA1 exerts activity of oncogenes in PTC through regulating miR-204/IGFBP5 axis.
Keywords: papillary thyroid carcinoma, lncRNA, UCA1, miR-204, IGFBP5