LINC00665 functions as a competitive endogenous RNA to regulate AGTR1 expression by sponging miR‑34a‑5p in glioma.

Glioma is the most aggressive tumor of the central nervous system. Long non‑coding RNAs (lncRNAs) may be involved in modulating tumor generation. The present study analyzed an lncRNA microarray of glioma and selected long intergenic non‑protein coding RNA 665 (LINC00665) as the research object. The mode of expression and biological function of LINC00665 in glioma were assessed using lncRNA microarray and RT‑qPCR analyses. Gain‑of‑function assays and/or loss‑of‑function assays were implemented to explore the role of LINC00665 in the progression of glioma. Dual‑luciferase reporter and RNA immunoprecipitation assays explored the downstream molecular mechanism of LINC00665. The function of the molecular pathway in progression of glioma was analyzed using rescue assays. High expression of LINC00665 was marked in glioma tissues and cells, which correlated with an unsatisfactory prognosis. Upregulation of LINC00665 significantly promoted the proliferation and invasion of glioma cells. LINC00665 acted as a competing endogenous RNA by sponging miR‑34a‑5p to upregulate angiotensin II receptor type 1 (AGTR1). LINC00665 promoted the progression of glioma by acting as a competitive endogenous RNA to competitively bind to miR‑34a‑5p and mediate AGTR1 expression.