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Intracranial aneurysm (IA) is a devastating disease, the pathogenesis of which remains to be elucidated. The present study aimed to determine the molecular mechanism of IA and to identify potential therapeutic targets using bioinformatics analysis. The GSE54083 dataset, which includes data from patients with ruptured IA and superficial temporal artery controls, was downloaded from the Gene Expression Omnibus, and differentially expressed genes (DEGs) were identified in the ruptured IA samples using the limma package in R. Subsequently, the Database for Annotation, Visualization and Integrated Discovery software was used to perform function and pathway enrichment analyses and the Search Tool for the Retrieval of Interacting Genes database was used to construct the protein‑protein interaction (PPI) network. Then, microRNA (miRNA) target and transcription factor (TF) target pairs were identified using the miR2Disease, MiRwalk2, ITFP and TRANSFAC databases. Finally, an integrated network of TF‑target‑miRNAs was constructed using Cytoscape. A total of 402 upregulated DEGs and 375 downregulated DEGs were identified from the ruptured IA samples compared with the superficial temporal artery samples. The majority of the upregulated DEGs were significantly enriched in the immune system development category, including CD40 ligand (CD40LG) and CD40 and the downregulated DEGs, such as striatin (STRN), were enriched in neuron projection development. In addition, nitric oxide synthase 1 (NOS1), a target of miRNA‑125b, and myosin heavy chain 11 (MYH11), a target of minichromosome maintenance complex component 4 (MCM4), had higher degree scores in the integrated network. These findings suggest that CD40, CD40LG, NOS1, STRN, MCM4, MYH11 and miR‑125b may be potential therapeutic targets for the treatment of IA.

Accumulating evidence suggests that microRNA (miR)-146a functions as an oncogene or tumor suppressor in various cancers. However, the role of miR‑146a in gastric cancer (GC) remains to be elucidated. The present study investigated the function of miR‑146a in GC cells. The results of the present study revealed that miR‑146a modulates GC cell apoptosis. Overexpression of miR‑146a significantly increased apoptosis of SGC‑7901 cells, whereas inhibition of miR‑146a protected cells from apoptosis. miR‑146a expression in GC cells was inversely correlated with transforming growth factor β‑activated kinase 1 (TAK1) expression, at the mRNA and protein levels. Furthermore, small interfering RNA‑mediated silencing of TAK1 enhanced GC cell apoptosis, whereas overexpression of TAK1 promoted survival of GC cells. Overexpression of miR‑146a or knockdown of TAK1 led to a marked increase in inhibitor of κBα (IκBα) and a decrease in B‑cell lymphoma 2 (Bcl‑2) expression levels in SGC‑7901 cells. By contrast, silencing of miR‑146a or TAK1 overexpression downregulated IκBα and upregulated Bcl‑2 expression levels. Therefore, the results of the present study demonstrated a novel negative feedback mechanism to promote GC cell apoptosis involving the miR‑146a/TAK1/nuclear factor-κB axis.

Osteosarcoma is the most common primary bone tumor characterized by high risk of metastasis, thus presents with an overall survival rate of 60%, despite the use of chemotherapy and surgery. Metastasis‑associated lung adenocarcinoma transcript 1 (MALAT‑1) has been reported to upregulated and epigenetically regulate the metastasis in osteosarcoma; however, the regulatory mechanisms of MALAT‑1 expression remain unclear. In the current study, significant upregulation of MALAT‑1 was observed subsequent to exposure to low concentrations of 17β‑estradiol (E2) in U2OS cells. Using chromatin immunoprecipitation assays, E2‑activated estrogen receptor α (ERα) was identified to promote the binding of specificity protein 1 (Sp1) to the MALAT‑1 promoter. Electrophoretic mobility shift assay and immunoprecipitation results demonstrate that ERα binds indirectly to the MALAT‑1 promoter by binding directly to Sp1 protein. Notably, without E2 stimulation, overexpressed ERα results in no significant promotion of the Sp1/MALAT‑1 promoter, indicating that the translocation of ERα to nuclei stimulated by E2 is necessary. The immunofluorescence assay confirmed that E2 stimulation promotes the translocation of Sp1 to the nuclei in an ERα‑dependent manner. Subsequently, the effects of E2 on osteosarcoma physiological processes were further analyzed. Consistently, E2 treatment was observed to promote proliferation, colony formation, migration and invasion in U2OS cells. Taken together, the results indicate a role for E2 in regulating the physiological processes of osteosarcoma cells by regulating MALAT‑1 expression levels.