Purpose
Recent studies have identified important roles for
long intergenic non-protein coding RNA 1426
(
LINC01426
) in glioma and clear cell renal cell carcinoma. The present study evaluated the expression profile of
LINC01426
in non-small cell lung cancer (NSCLC) tissues and cell lines. Furthermore, the function of
LINC01426
in NSCLC and the molecular mechanisms involved were extensively studied.
Methods
The abundance of
LINC01426
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
LINC01426
in NSCLC cells. Mechanistic studies were performed using the luciferase reporter assay and RNA immunoprecipitation.
Results
Significant
LINC01426
upregulation was observed in NSCLC tissues and cell lines. Silencing
LINC01426
inhibited proliferation, migration, and invasion of NSCLC cells and facilitated cell apoptosis in vitro. Furthermore, interference of
LINC01426
restricted tumor growth of NSCLC cells in vivo. In addition,
LINC01426
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
ETS proto-oncogene 1
(
ETS1
) was identified as a direct target of miR-519d-5p and
LINC01426
could indirectly upregulate
ETS1
expression by sponging miR-519d-5p. Moreover, the cancer-inhibiting activities of
LINC01426
knockdown in NSCLC cells were partially offset by miR-519d-5p inhibition.
Conclusion
LINC01426
increases
ETS1
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.