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-κB (NF-κB) p65, p-NF-κB p65 and inhibitor of κBα (IκBα) 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-κB 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-κB pathway. CONCLUSION: LIFR-AS1 could suppress the proliferation, migration and invasion and promote the apoptosis through modulating miR-4262/NF-κB pathway in glioma.

Activation of astrocytes and expression of inflammatory cytokines in rats with experimental autoimmune encephalomyelitis.

The aim of the study was to investigate and discuss the activation of astrocytes and the expression of inflammatory cytokines in rats with experimental autoimmune encephalomyelitis (EAE). Twenty Wistar rats were randomly divided into the normal control (n=10) and EAE group (n=10). The rats in the EAE group were injected intraperitoneally with myelin oligodendrocyte glycoprotein 35-55 emulsion, and those in the control group were injected with the equivalent volume of normal saline. Wear neurological function scale was applied to evaluate the neurological functions of the rats, and the weight changes were recorded. At 21 days after immunization, hematoxylin and eosin staining was used to detect the histomorphology, and immunofluorescence was used to measure the activation conditions of the brain astrocytes. Reverse transcription-polymerase chain reaction and western blot analysis were utilized to detect the messenger RNA (mRNA) and protein levels of inflammatory factors. The disease occurred in rats of the EAE group at 9 days after immunization, and the incidence rate was 80%. The Wear score of the rats in the EAE group was significantly increased compared with that in the control group (P<0.05). At 9 days after immunization, the weight of the rats in the EAE group was obviously lower than that in the control group (P<0.05). The inflammatory lesion of rats in the EAE group mainly occurred in the region of brain parenchyma. The glial fibrillary acidic protein level in the brain sections of the rats in the EAE group was markedly elevated compared with that in control group. The mRNA and protein levels of interleukin-10 in the rat brain in EAE group were decreased notably (P<0.05), while those of interferon-γ and tumor necrosis factor-α were increased significantly (P<0.05). The significant increases in the activation level of astrocytes and inflammatory cytokine level have a close relationship with EAE progression.