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.

Exosomal miRNA-128-3p from mesenchymal stem cells of aged rats regulates osteogenesis and bone fracture healing by targeting Smad5

“…For example, it was reported that miR-128-3p suppressed breast cancer progression by targeting LIM domain kinase 1(LIMK1) [68]. Furthermore, miR-128-3p was demonstrated to inhibit glioma cell proliferation and differentiation through the IRS-1/PI3K/AKT signaling pathway [69]. Exosome-transmitted miR-128-3p could also exert its anticancer effect by increasing the chemosensitivity of oxaliplatin-resistant colorectal cancer [70].…”

Potential role of lncRNA HULC/miR‑128‑3p/RAC1 axis in the inflammatory response during LPS‑induced sepsis in HMEC‑1 cells

“…Selenium could mitigate lPS-induced myocardial inflammation by modulating the mir-128-3p/p38MaPK-nF-κB pathway (31). mir-128-3p also functions as a tumor suppressor in human breast cancer (32), glioma (33) and hepatocellular carcinoma (34). in the present study, mir-128-3p interference aggravated lPS-mediated damage in HMec-1 cells, and abolished the Hulc knockdown-mediated reduction of apoptosis and expression levels of proinflammatory cytokines in LPS-treated HMEC-1 cells.…”

Long noncoding RNA HOTTIP is associated with male infertility and promotes testicular embryonal carcinoma cell proliferation

“…The above results imply that HOTTIP can be directly combined with miR‐128‐3p and considered as a ceRNA. Numerous studies in recent years have confirmed that miR‐128‐3p can inhibit cell proliferation level (Huang et al, ; Huo et al, ; Zhou et al, ). The current research pointed out that miR‐128‐3p expression in testicular samples from Hypo patients was notably increased.…”