Dysregulation of microRNA‑23b‑3p contributes to the development of intracranial aneurysms by targeting phosphatase and tensin homolog.

MicroRNA‑23b‑3p (miR‑23b‑3p) has been reported to be involved in the pathogenesis of a number of diseases, including non‑small cell lung cancer and gastric cancer, by acting on different signaling pathways. The present study aimed to understand the association between the miR‑23b‑3p level of intracranial aneurysms (IAs) and the mechanism involved. Computational analysis was used to search for the target of miR‑23b‑3p, and luciferase assay was used to validate the miRNA/target association. Western blot analysis and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) were used to determine the expression of miR‑23b‑3p and phosphatase and tensin homolog (PTEN), and their expression in smooth muscle cells (SMCs) treated with miRNA mimic or inhibitor. Firstly, an online miRNA database (www.mirdb.org) was searched using the 'seed sequence' located within the 3'‑untranslated region of the target gene, and then PTEN was validated as the direct target gene via a luciferase reporter assay system. The negative regulatory association between miR‑23b‑3p and PTEN was determined through the analysis of the relative luciferase activity. Additionally, RT-qPCR and western blot analysis was performed in order to assess the mRNA and protein expression levels of PTEN among IA (n=32) and control (n=17) groups or cells treated with scramble control, miR‑23b‑3p mimics, PTEN siRNA and miR‑23b‑3p inhibitors to verify the negative regulatory association between miR‑23b‑3p and PTEN. Experiments were then performed to investigate the effect of miR‑23b‑3p and PTEN on the viability and apoptosis of pulmonary artery SMCs (PASMCs). The results showed that cells transfected with miR‑23b‑3p inhibitors suppressed the viability of SMCs by promoting the apoptosis of the cells compared with that of the scramble controls, while cells transfected with miR‑23b‑3p mimics and PTEN siRNA enhanced the viability of VSMCs by inducing apoptosis. This indicated that miR‑23b‑3p negatively interfered with the viability of the cells, while PTEN positively interfered with the viability of the cells. In conclusion, PTEN was found to be a virtual target of miR‑23b‑3p, and a negative regulatory association existed between miR‑23b‑3p and PTEN. miR‑23b‑3p and PTEN interfered with the viability and apoptosis of SMCs.