Long Noncoding RNA LINC01426 Sequesters microRNA-519d-5p to Promote Non-Small Cell Lung Cancer Progression by Increasing ETS1 Expression.

PURPOSE

Recent studies have identified important roles for () in glioma and clear cell renal cell carcinoma. The present study evaluated the expression profile of in non-small cell lung cancer (NSCLC) tissues and cell lines. Furthermore, the function of in NSCLC and the molecular mechanisms involved were extensively studied.

METHODS

The abundance of in NSCLC tissues and cell lines was determined using quantitative reverse transcription-polymerase chain reaction. The cell counting kit-8 assay, flow cytometry, transwell experiments for migration and invasion, and xenograft tumor model were used to assess the function of in NSCLC cells. Mechanistic studies were performed using the luciferase reporter assay and RNA immunoprecipitation.

RESULTS

Significant upregulation was observed in NSCLC tissues and cell lines. Silencing inhibited proliferation, migration, and invasion of NSCLC cells and facilitated cell apoptosis in vitro. Furthermore, interference of restricted tumor growth of NSCLC cells in vivo. In addition, showed the ability to directly bind to microRNA-519d-5p (miR-519d-5p) and act as a molecular sponge for miR-519d-5p in NSCLC cells. Furthermore, the () was identified as a direct target of miR-519d-5p and could indirectly upregulate expression by sponging miR-519d-5p. Moreover, the cancer-inhibiting activities of knockdown in NSCLC cells were partially offset by miR-519d-5p inhibition.

CONCLUSION

increases expression by sequestering miR-519d-5p, thereby aggravating the malignant progression of NSCLC. The LINC01426/miR-519d-5p/ETS1 competing endogenous RNA pathway may provide a target for designing therapeutic agents for NSCLC treatment.