Abstract
Papillary thyroid carcinoma (PTC) is a common malignancy worldwide. LncRNA LINC00704 (mitotically associated long non-coding RNA) was reported as a crucial regulator in PTC. However, the biological mechanism of LINC00704 action remains unclear in PTC. The mRNA levels of LINC00704, miR-204-5p, and high-mobility group box 1 (HMGB1) were measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assay. HMGB1, proliferating cell nuclear antigen (PCNA), and cyclin D1 protein levels were detected using the Western blot assay. The binding relationship between miR-204-5p and LINC00704 or HMGB1 was predicted by LncBase Predicted v.2 or TargetScan, respectively, and then validated by dual luciferase reporter assay. Cell viability, cell cycle, cell migration and invasion, and migration ratio were assessed by MTT, flow cytometry, transwell cell migration and invasion, and wound-healing assays, respectively. Results suggested that LINC00704 and HMGB1 were elevated and miR-204-5p decreased in PTC tissues and cells. Furthermore, rescue experiments demonstrated that the miR-204-5p inhibitor alleviated the inhibitory effects of LINC00704 knockdown on cell proliferation, cell cycle, migration, and invasion. Meanwhile, miR-204-5p overexpression repressed proliferation, migration, and invasion by targeting HMGB1. Mechanical analysis discovered that LINC00704 could act as an miR-204-5p sponge to modulate HMGB1 expression. In conclusion, LINC00704 promoted PTC cell proliferation, cell cycle, migration, and invasion by the miR-204-5p/HMGB1 axis, providing a novel therapeutic target for PTC patients.