lnc-NLC1-C inhibits migration, invasion and autophagy of glioma cells by targeting miR-383 and regulating PRDX-3 expression

Long non-coding RNAs (lncRNAs) serve an important role in tumor progression, and their abnormal expression is associated with tumor development. The lncRNA narcolepsy candidate region 1 gene C (lnc-NLC1-C) is involved in numerous types of cancer, but its biological function in glioma remains unknown. In the present study, lnc-NLC1-C expression was detected using reverse transcription-quantitative (RT-q)PCR in U251, SHG44, U87MG and U118MG glioma cells. U87MG cells were transfected with lnc-NLC1-C overexpression or interference vectors. Cell proliferation was detected using a Cell Counting Kit-8 assay. Cell migration and invasion were examined using a Transwell assay, while apoptosis, cell cycle and reactive oxygen species production were evaluated using flow cytometry, and the expression levels of lnc-NLC1-C, microRNA (miR)-383 and peroxiredoxin 3 (PRDX-3) were measured using western blotting and RT-qPCR. Rescue experiments were performed to verify the function of the lnc-NLC1-C/miR-383/PRDX-3 axis. The highest expression levels of lnc-NLC1-C were identified in U87MG glioma cells. Overexpression of lnc-NLC1-C expression promoted cell proliferation, G(1) phase blocking, migration and invasion, while inhibiting apoptosis and autophagy in U87MG cells. Mechanistically, miR-383 could bind to lnc-NLC1-C to regulate PRDX-3 expression and improve its oncogenic effect. Rescue experiments confirmed that the lnc-NLC1-C/miR-383/PRDX-3 axis was involved in the molecular mechanism of glioma progression. Therefore, lnc-NLC1-C may be a tumor promoter that affects multiple biological functions, such as migration, invasion and autophagy, in glioma cells.

Automated summary

The study revealed that lnc-NLC1-C is highly expressed in glioma cells, and its overexpression promotes cell proliferation, migration, and invasion while inhibiting apoptosis and autophagy. miR-383 binds to lnc-NLC1-C to regulate PRDX-3 expression, enhancing its oncogenic effect.