Bin Liu1, Wei Cao1, Hui Ma1. 1. a Department of Neurosurgery, Jining No.1 People's Hospital , Jining , China.
Abstract
Background: Glioma is a main cause of brain-cancer relevant death. The present paper designed to reveal the possible role of LSINCT5 in human glioma GL15 cells. Methods: LSINCT5 and miR-451 expression in glioma tissues was examined using qRT-PCR. The impacts of LSINCT5, miR-451 and Rac1 in GL15 cells were checked by carrying out CCK-8 assay, transwell assay, and flow cytometric analysis. Further, the target gene of LSINCT5 and miR-451 was explored. Accumulation of PI3K/AKT, Wnt/β-catenin and NF-κB pathway proteins was examined using Western blot. Results: LSINCT5 was highly expressed while miR-451 low expressed in glioma tissues when compared to normal controls. Down-regulating LSINCT5 effectively declined GL15 cells viability, migration and invasion, but accelerated apoptosis. Nonetheless, the above-mentioned effects of LSINCT5 down-regulation were weakened when miR-451 was silenced. Rac1 was a target of miR-451. The tumour-suppressive effects of miR-451 on GL15 cells were weakened when Rac1 was overexpressed. Further, LSINCT5-miR-451-Rac1 axis could impact the activation of PI3K/AKT, Wnt/β-catenin and NF-κB pathways. Conclusion: Down-regulation of LSINCT5 represses glioma cells growth and metastasis in vitro likely through targeting miR-451 and thereby inhibiting Rac1-regulated PI3K/AKT, Wnt/β-catenin and NF-κB pathways.
Background: Glioma is a main cause of brain-cancer relevant death. The present paper designed to reveal the possible role of LSINCT5 in humanglioma GL15 cells. Methods:LSINCT5 and miR-451 expression in glioma tissues was examined using qRT-PCR. The impacts of LSINCT5, miR-451 and Rac1 in GL15 cells were checked by carrying out CCK-8 assay, transwell assay, and flow cytometric analysis. Further, the target gene of LSINCT5 and miR-451 was explored. Accumulation of PI3K/AKT, Wnt/β-catenin and NF-κB pathway proteins was examined using Western blot. Results:LSINCT5 was highly expressed while miR-451 low expressed in glioma tissues when compared to normal controls. Down-regulating LSINCT5 effectively declined GL15 cells viability, migration and invasion, but accelerated apoptosis. Nonetheless, the above-mentioned effects of LSINCT5 down-regulation were weakened when miR-451 was silenced. Rac1 was a target of miR-451. The tumour-suppressive effects of miR-451 on GL15 cells were weakened when Rac1 was overexpressed. Further, LSINCT5-miR-451-Rac1 axis could impact the activation of PI3K/AKT, Wnt/β-catenin and NF-κB pathways. Conclusion: Down-regulation of LSINCT5 represses glioma cells growth and metastasis in vitro likely through targeting miR-451 and thereby inhibiting Rac1-regulated PI3K/AKT, Wnt/β-catenin and NF-κB pathways.