RESUMO
BACKGROUND: Long non-coding RNA (LncRNA) is associated with disease progression. It is reported that LINC01087 is highly expressed in cancer and participates in tumorigenesis. However, whether it regulates the development of glioma has not been studied. So, the goal of this research is to determine the role of LINC01087 in gliomas and to provide potential targets for clinical treatment. METHODS: The gene expression was detected by quantitative reverse transcriptase polymerase chain reaction (QRT-PCR) and Western blotting (WB). Cell proliferation was analyzed by CCK8 and colony formation test, and apoptosis was detected by flow cytometry. Luciferase report experiment and RNA Binding Protein Immunoprecipitation confirmed the interaction between LINC01087, miR-384 and Bcl-2. The effect of regulating LINC01087 on the growth of glioma was confirmed in vitro. RESULTS: The LINC01087 expression was up-regulated in clinical glioma samples (n = 35). Furthermore, LINC01087 silencing can obviously suppress the proliferation of glioma cells and induce apoptosis. Mechanically, we found that LINC01087 was the molecular sponge of miR-384. LINC01087 could inhibit the miR-384 expression and boost the Bcl-2 expression through sponge expression of miR-384. The repair of Bcl-2 effectively saved the proliferation and apoptosis of glioma cells lacking LINC01087. CONCLUSION: LINC01087 is highly expressed in glioma and can participate in the growth of glioma through miR-384/Bcl-2 axis. So, it is a potential therapeutic target.
Assuntos
Neoplasias Encefálicas/genética , Carcinogênese/genética , Regulação Neoplásica da Expressão Gênica , Glioma/genética , MicroRNAs/metabolismo , Proteínas Proto-Oncogênicas c-bcl-2/genética , RNA Longo não Codificante/metabolismo , Adulto , Animais , Apoptose , Encéfalo/metabolismo , Encéfalo/patologia , Neoplasias Encefálicas/metabolismo , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Progressão da Doença , Feminino , Glioma/metabolismo , Humanos , Masculino , Camundongos , Camundongos Nus , Pessoa de Meia-Idade , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Regulação para Cima , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
The aim of the present study was to investigate the protective effect of chicoric acid on oxidative stress and inflammation in rats with cerebral ischemia-reperfusion injury. A cerebral ischemia-reperfusion injury rat model was created via transient middle cerebral artery occlusion (MCAO) and rats were treated with various doses of chicoric acid (0, 1, 10 and 100 mg/kg). Neurological deficits and infarct volume were used to estimate the protective effects of chicoric acid treatment. Levels of reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, nitric oxide (NO) and prostaglandin E2 (PGE2) were assessed. Western blot analysis was also used to measure the expression of cyclooxygenase (COX)-2, p38-mitogen activated protein kinase (MAPK), c-Jun, phosphorylated protein kinase B (p-AKT) and AKT. Chicoric acid exposure was observed to reduce neurological deficits and infarct volume in rats with cerebral ischemia-reperfusion injury. In addition, ROS production and inflammation were significantly suppressed following treatment with chicoric acid. Chicoric acid was demonstrated to significantly inhibit the upregulation of NO and PGE2 levels in rats following MCAO. Furthermore, chicoric acid significantly suppressed the MCAO-induced promotion of COX-2, p38-MAPK and c-Jun protein expression and enhanced the inhibition of p-AKT/AKT. These results suggest that chicoric acid has a protective effect, preventing oxidative stress and inflammation in rats with cerebral ischemia-reperfusion injury via the p38-MAPK, c-Jun and AKT signaling pathways.
