Long non‑coding RNA NORAD promotes cell proliferation and glycolysis in non‑small cell lung cancer by acting as a sponge for miR‑136‑5p.

Abstract

NORAD (non-coding RNA activated by DNA damage) is a long non-coding RNA (lncRNA) that is upregulated and promotes cell progression in various human types of cancer; however, its function in non-small cell lung cancer (NSCLC) remains unclear. The present study investigated the regulatory function and underlying mechanisms of NORAD in NSCLC. NORAD and miR-136-5p expression were assessed by reverse transcription-quantitative polymerase chain reaction, and proliferation and glycolysis-associated markers were also assessed. Direct miR-136-5p regulation by NORAD was detected using luciferase reporter assay and RNA immunoprecipitation. NORAD was highly expressed in NSCLC tissues and cell lines. NORAD overexpression increased NSCLC proliferation and glycolysis. Further investigation revealed that NORAD serves as a competing endogenous RNA for miR-136-5p. Gain- and loss-of-function experiments confirmed that miR-136-5p reversed the promoting effects of NORAD in NSCLC. Results of the present study indicate that NORAD serves as a growth-promoting lncRNA in NSCLC by suppressing the function of miR-136-5p. NORAD and miR-136-5p interaction may provide a potential target for NSCLC treatment.