LINC00606 regulates glioblastoma progression by sponging miR-486-3p and interacting with ATP11B

Abstract Background LncRNAs regulate tumorigenesis and development in a variety of cancers; nevertheless, the biological functions and molecular mechanisms of LINC00606 in glioblastoma (GBM) remain largely unknown. Methods The expression of LINC00606 and ATP11B in glioma and normal brain tissues was evaluated by qPCR, and the biological functions of the LINC00606/miR-486-3p/TCF12/ATP11B axis in GBM were verified through a series of in vitro and in vivo experiments. The molecular mechanism of LINC00606 was revealed by immunoblotting, FISH, RNA pulldown, CHIP-qPCR, and a dual-luciferase reporter assay. Results LINC00606 is highly expressed in GBM patient samples and is related to the poor prognosis. Here, LINC00606 promoted the proliferation, clonal expansion, and migration of glioma cells and reduced the levels of apoptosis. LINC00606 targets TCF12 by sponging miR-486-3p, which has been proven to affect the transcriptional initiation of LINC00606, PTEN, and KLLN. In addition, by working in concert with ATP11B, LINC00606 regulates the PI3K/AKT signaling pathway to mediate the proliferation, migration, and apoptosis of glioma cells. Conclusion The LINC00606/miR-486-3p/TCF12/ATP11B axis is involved in the regulation of glioma progression and plays a specific regulatory role at both the transcriptional and post-transcriptional levels via the sponging of miR-486-3p by LINC00606 to target TCF12 and the interaction of LINC00606 with ATP11B, interference with which may prove to be a new strategy for the treatment of glioblastoma.