Long noncoding RNA LIFR-AS1 suppresses proliferation, migration and invasion and promotes apoptosis through modulating miR-4262/NF-κB pathway in glioma

Aim: This study aimed to explore the role of lncRNA leukemia inhibitory factor receptor antisense RNA 1 (LIFR-AS1) on glioma and its underlying molecular mechanism. Methods: The expression of LIFR-AS1 and miR-4262 was detected by quantitative real-time polymerase chain reaction (qRT-RCR) in both glioma tissues and cell lines. Colony formation assay, 5-ethynyl-20-deoxyuridine (EdU) assay, flow cytometry and transwell assay were respectively conducted to detect cell clones, proliferation, apoptosis, migration and invasion. The effect of LIFR-AS1 on the chemoresistance to temozolomide (TMZ) of glioma cells was also analyzed. In addition, dual-luciferase reporter gene assay was performed to evaluate the luciferase activity. The expressions of nuclear factor-kappa B (NF-kappa B) p65, p-NF-kappa B p65 and inhibitor of kappa B alpha (I kappa B alpha) in glioma cells were measured by western blot. Results: LIFR-AS1 was lowly expressed and miR-4262 was highly expressed in glioma tissues and cell lines. LIFR-AS1 overexpression inhibited the proliferation, migration and invasion and promoted apoptosis of glioma cells. LIFR-AS1 overexpression also reduced the chemoresistance to TMZ of glioma cells. Moreover, LIFR-AS1 overexpression suppressed the activation of NF-kappa B signaling pathway in glioma cells. miR-4262 was the target gene of LIFR-AS1. We also found that miR-4262 abrogated the functions of LIFR-AS1 on cell proliferation, apoptosis, migration and invasion of glioma cells in the NF-kappa B pathway. Conclusion: LIFR-AS1 could suppress the proliferation, migration and invasion and promote the apoptosis through modulating miR-4262/NF-kappa B pathway in glioma.

Automated summary

The study found that LIFR-AS1 was underexpressed and miR-4262 was overexpressed in glioma tissues and cell lines. Overexpression of LIFR-AS1 inhibited glioma cell proliferation, migration, and invasion, and promoted apoptosis. Additionally, LIFR-AS1 overexpression reduced chemoresistance to TMZ and suppressed NF-kappa B signaling pathway activation in glioma cells.