Long Intergenic Non-Protein Coding RNA 519 Promotes the Biological Activities of Tongue Squamous Cell Carcinoma by Sponging microRNA-876-3p and Consequently Upregulating MACC1.

PURPOSE

Long intergenic non-protein coding RNA 519 () promotes the development of lung squamous cell carcinoma. In this study, we detected the expression of in tongue squamous cell carcinoma (TSCC) and examined its clinical significance. Additionally, the regulatory effects of on behaviors of TSCC tumor cells were explored through functional experiments. Finally, mechanistic studies were performed to elucidate the molecular events underlying the tumor-promoting actions of in TSCC.

MATERIALS AND METHODS

The expression of in TSCC tissues and cell lines was determined using quantitative reverse transcription-polymerase chain reaction. Cell counting kit-8 assay, flow cytometric analysis, cell migration and invasion assays and xenograft tumor model analyses were used to detect TSCC cell proliferation, apoptosis, migration and invasion and in vivo tumor growth, respectively. Mechanistic studies were performed using bioinformatics analysis, RNA immunoprecipitation assay, luciferase reporter assay and rescue experiments.

RESULTS

was overexpressed in both TSCC tissues and cell lines. A high level was associated with poor overall survival in patients with TSCC. In vitro, played cancer-promoting roles in TSCC progression by facilitating cell proliferation, migration and invasion and restraining cell apoptosis. In vivo, downregulation resulted in decreased TSCC tumor growth. Mechanistically, acted as a competing endogenous RNA for microRNA-876-3p (miR-876-3p), which directly targets metastasis associated with colon cancer-1 (), in TSCC cells. upregulated the expression of in TSCC cells by sequestering miR-876-3p. Rescue experiments further affirmed that miR-876-3p inhibition or overexpression mitigated the inhibitory influences of depletion on cell proliferation, migration and invasion and neutralized the promoting actions of knockdown on cell apoptosis in TSCC.

CONCLUSION

aggravated the oncogenicity of TSCC by regulating the miR-876-3p/MACC1 axis. Our findings suggest that the LINC00519/miR-876-3p/MACC1 pathway may be an underlying therapeutic target in TSCC.