LINC00294 negatively modulates cell proliferation in glioma through a neurofilament medium-mediated pathway via interacting with miR-1278.

BACKGROUND

Accumulating long noncoding RNAs (lncRNAs) have been recognized to participate in glioma development. Nevertheless, knowledge of the role of linc00294 in glioma remains incomplete.

METHODS

Bioinformatics analysis predicted the differential expression of LINC00294 and neurofilament medium (NEFM) in tumors and normal tissues, as well as the binding between LINC00294 and miR-1278, miR-1278 and NEFM. Luciferase and RNA immunoprecipitation assays were used for the verification of interactions. The potential role of LINC00294 in glioma development was investigated using functional assays, singly and in parallel with its interplay with miR-1278 and NEFM. Cell counting kit-8 and EdU assays were applied to measure cellular proliferation, whereas the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method was employed to detect apoptosis.

RESULTS

A new lncRNA, LINC00294, was highly expressed in normal brain tissues. However, it was markedly down-regulated in GBM tissues and glioma cell lines. Overexpression of LINC00294 abates glioma cell proliferation but induces apoptosis. Meanwhile, tumor suppressor NEFM was revealed to be distinctly diminished in cancerous conditions and enhanced in glioma cells by LINC00294 up-regulation. Interactions of miR-1278 with LINC00294 or NEFM occur, and the expression of NEFM is up-regulated by LINC00294 through their competition with respect to binding to miR-1278. Finally, the rescue assays further confirmed that LINC00294 inhibits glioma cell proliferation by absorbing miR-1278 to enhance NEFM.

CONCLUSIONS

Collectively, our observations demonstrate the tumor-suppressive function of LINC00294 in glioma development by sponging miR-1278 and promoting NEFM, suggesting a potential use in therapy for glioma.