Abstract

Previously, a number of microRNAs (miRs) have been identified to participate in the development and progression of glioma via the regulation of their target genes. However, the molecular mechanisms underlying the effect of miR-423-3p in glioma growth remain unclear. In the present study, the reverse transcription-quantitative polymerase chain reaction and western blotting were used to assess the mRNA and protein expression levels of miR-423-3p, respectively. An MTT assay and flow cytometry were performed to determine cell proliferation and apoptosis, respectively. A luciferase reporter gene assay was performed to determine the target association between pannexin 2 (PANX2) and miR-423-3p. It was revealed that miR-423-3p was significantly upregulated in glioma tissues compared with normal brain tissues, and the increased expression of miR-423-3p was significantly associated with an advanced grade as well as a poorer prognosis of patients with glioma. Inhibition of miR-423-3p using an miR-423-3p inhibitor resulted in the decreased proliferation of glioma U251 and U87MG Uppsala cells, and the induction of apoptosis. PANX2 was identified as a novel target gene of miR-423-3p, and the expression of PANX2 was revealed to be increased in U251 and U87MG Uppsala cells when miR-423-3p was inhibited. Knockdown of PANX2 attenuated the effects of miR-423-3p inhibition on glioma cell proliferation and apoptosis. Furthermore, PANX2 was significantly downregulated in glioma tissues compared with normal brain tissues, and its levels were markedly lower in World Health Organization (WHO) stage III–IV gliomas compared with WHO stage I–II gliomas. Additionally, the expression levels of PANX2 were identified to be inversely correlated with miR-423-3p expression levels in glioma tissues. Consequently, targeting miR-423-3p may inhibit glioma growth via the upregulation of PANX2.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call