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MiR-128-3p inhibits glioma cell proliferation and differentiation by targeting NPTX1 through IRS-1/PI3K/AKT signaling pathway.

ABSTRACT: It has been reported that glioma has a higher morbidity and mortality than other types of malignant brain tumor. While glioma has been extensively researched, the exact molecular mechanisms of its genesis and progression have remained to be fully elucidated. In order to explore a novel glioma-associated pathway which may represent a therapeutic target, 61 pairs of tumor tissues and adjacent normal tissues of glioma patients were collected and subjected to reverse-transcription quantitative polymerase chain reaction analysis, indicating that the relative expression of microRNA (miR)-128-3p was significantly decreased in the tumor tissues. However, the expression of neuronal pentraxin 1 (NPTX1) was obviously elevated. Through a bioinformatics analysis using Targetscan and transfection experiments, it was confirmed that NPTX1 was targeted by miR-128-3p. In the U251 human glioma cell line, transfection with miR-128-3p mimics increased the levels of phosphorylated insulin receptor substrate 1 (p-IRS-1), phosphoinositide-3 kinase (PI3K) and p-AKT, as demonstrated by western blot analysis. In addition, the proliferation rate of the cells was notably decreased following transfection with miR-128-3p mimics. Conversely, transfection with miR-128-3p inhibitor significantly increased the levels of p-IRS-1, PI3K and p-AKT, accompanied by an elevated proliferation rate of the cells. Therefore, it was indicated that miR-128-3p could reversely regulate NPTX1 expression. After the expression of NPTX1 was inhibited with specific small interfering RNA, the levels of p-IRS-1, PI3K and p-AKT were obviously decreased, while the expression of miR-128-3p was not significantly changed. Overall, it was concluded that miR-128-3p suppresses glioma through the NPTX1/IRS-1/PI3K/AKT signaling pathway.

SUBMITTER: Huo L

PROVIDER: S-EPMC6425241 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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miR-128-3p inhibits glioma cell proliferation and differentiation by targeting NPTX1 through IRS-1/PI3K/AKT signaling pathway.

Huo Leiming L Wang Bin B Zheng Maohua M Zhang Yonghong Y Xu Jiguang J Yang Gang G Guan Quanlin Q

Experimental and therapeutic medicine 20190218 4

It has been reported that glioma has a higher morbidity and mortality than other types of malignant brain tumor. While glioma has been extensively researched, the exact molecular mechanisms of its genesis and progression have remained to be fully elucidated. In order to explore a novel glioma-associated pathway which may represent a therapeutic target, 61 pairs of tumor tissues and adjacent normal tissues of glioma patients were collected and subjected to reverse-transcription quantitative polym ...[more]

PMID: 30906475

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Project description:BackgroundThe incidence of nasopharyngeal carcinoma is increasing gradually, but the pathogenesis is not completely clear. MicroRNA, a highly conserved endogenous noncoding small molecule RNA, plays an essential role in the regulation of gene expression and is a hotspot in cancer research worldwide.ObjectivesAlthough previous studies have confirmed that the abnormal expression of microRNAs is closely related to the progression of nasopharyngeal carcinoma, the role of miRNA-331-3p in nasopharyngeal carcinoma has not been studied. The purpose of this study was to explore the role and mechanism of miRNA-331-3p in the progression of nasopharyngeal carcinoma.Materials and methodsReal-time quantitative reverse transcription polymerase chain reaction was performed to detect the expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cell lines (CNE-1 and 5-8F cells). After overexpression of miRNA-331-3p in CNE-1 cells, cell proliferation was measured by Cell Counting Kit-8 assay, cell invasion was detected by Transwell assay, and apoptosis was tested by flow cytometry. In addition, the dual-luciferase reporter assay was used to identify the target gene of miRNA-331-3p and Western blotting was performed to measure the relative protein expression.ResultsThe expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cells was decreased significantly. Overexpression of miRNA-331-3p markedly inhibited the proliferation and invasion of CNE-1 cells and promoted cell apoptosis. Moreover, overexpression of miRNA-331-3p reduced the expression of target gene elF4B, leading to inhibition of the phosphorylation of Phosphoinositide 3-kinase (PI3K) and Serine/ threonine kinase (AKT).ConclusionmiRNA-331-3p inhibited cell proliferation and induced cell apoptosis in nasopharyngeal carcinoma by targeting elF4B gene and then blocked the PI3K-AKT signaling pathway.SignificanceThe role of miRNA-331-3p in the development of NPC and its mechanism provide new ideas for the treatment of nasopharyngeal carcinoma.

Dataset Information

MiR-128-3p inhibits glioma cell proliferation and differentiation by targeting NPTX1 through IRS-1/PI3K/AKT signaling pathway.

Publications

miR-128-3p inhibits glioma cell proliferation and differentiation by targeting NPTX1 through IRS-1/PI3K/AKT signaling pathway.

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