Circular RNAs (circRNAs) play a role in various types of cancer. The present study suggested that hsa_circ_0026123 expression was upregulated in ovarian cancer (OVA), which was associated with its role in OVA. However, the role of hsa_circ_0026123 in OVA cell invasion and proliferation remains unclear. In the present study, OVA tissues and cell lines were used to investigate the functions of hsa_circ_0026123. The associations between hsa_circ_0026123, miR‑124‑3p and enhancer of zeste homolog 2 (EZH2) were examined using a luciferase reporter assay. RT‑qPCR and western blot analysis were used for gene and protein expression analysis, respectively. Tumor growth was detected using nude mouse tumor xenografts derived from SKOV3 cells, with or without hsa_circ_0026123 downregulation. The results confirmed that hsa_circ_0026123 expression was upregulated in OVA tissues and cell lines, while hsa_circ_0026123 silencing suppressed cell proliferation and migration; it also suppressed the expression of cancer stem cell (CSC) differentiation‑related markers in either in vivo or in vitro experiments. The data revealed that hsa_circ_0026123 downregulation suppressed EZH2 expression by miR‑124‑3p 'sponging', which was confirmed by rescue experiments and luciferase reporter assays. The results revealed that hsa_circ_0026123 silencing suppressed ovarian cancer cell progression via the miR‑124‑3p/EZH2 signaling pathway. Overall, the findings demonstrated that hsa_circ_0026123 knockdown inhibited OVA cell progression by regulating the miR‑124‑3p/EZH2 axis. This methodology may thus be used for the targeted therapy of OVA, as well as a candidate biomarker for the diagnosis and treatment of OVA.Immature ovarian teratocarcinoma (IOT) is a rare and malignant type of ovarian teratoma, and the molecular mechanisms underlying the pathogenesis and malignant phenotype of IOT remain uncharacterized. The present study examined a long non‑coding RNA (lncRNA), long‑chain intergenic non‑coding RNA324 (LINC00324), which may serve a crucial role in pathogenesis of IOT. According to the results, LINC00324 was upregulated in IOT tissues and cells, as determined by reverse transcription‑quantitative PCR, and its depletion impaired cell proliferation ability and improved cell apoptosis ability in IOT. Furthermore, LINC00324 acted as a miR‑214‑5p sponge to derepress cyclin dependent kinase 6 (CDK6), cyclin D1 (CCND1), murine double minute homolog 2 (MDM2), and mouse double minute 4 (MDM4) expression, thus increasing IOT cell proliferation and repressing apoptosis. Taken together, these results demonstrated that LINC00324 could serve as a competing endogenous RNA to facilitate IOT cell proliferation by regulation of miR‑214‑5p‑CDK6/CCND1/MDM2/MDM4 network, which possibly provide a novel therapeutic target for IOT.Endothelial monocyte‑activating polypeptide II (EMAP II) is a sensitive marker of neurotoxic injury, the expression of which increases significantly under conditions of stress, such as hypoxia or apoptosis. Studies have confirmed the extensive apoptosis of nerve cells in the brain following status epilepticus (SE), and the occurrence of SE can confer a hypoxic state on cells.  https://www.selleckchem.com/  The purpose of the present study was to observe the changes in the expression of EMAP II, and in the numbers and tight junction protein levels of microvascular endothelial cells in the hippocampus of rats with pilocarpine‑induced SE. The protein expression levels of EMAP II, CD31, zonula occludens 1 (ZO‑1) and occludin in the hippocampus were determined by immunofluorescence and western blot analyses. It was found that almost 75.6% of the rats in the SE group developed Racine stage IV‑V seizures at approximately 44.7±18.8 min after the pilocarpine administration, and the 24‑h mortality rate was almost 10.4%. The weight of the rats in the SE group was significantly decreased within 24 h following SE. Immunofluorescence staining revealed a low EMAP II expression in the hippocampus of the rats in the control group; however, the numbers of EMAP II‑positive cells were significantly increased in the SE group from 2 h to 21 days. The trend of EMAP II protein expression was consistent with that obtained with immunofluorescence staining. The numbers of CD31‑positive microvascular endothelial cells were significantly increased from 24 h to 21 days compared with the levels in the control group. The protein expression of ZO‑1 and occludin was most significantly decreased in the SE group. On the whole, the present study demonstrated that the expression of EMAP II in the rat hippocampus was upregulated in the SE model, which may promote angiogenesis and alter the TJ integrity of brain microvascular endothelial cells, with an increased number of CD31‑positive microvascular endothelial cells and a decreased expression of ZO‑1 and occludin.Gastric cancer (GC) is one of the most common malignancies and the second leading cause of cancer‑associated death in the world. The carcinogenesis and development of GC involves complicated steps and various factors, in which the tumor microenvironment serves a vital role. Mesenchymal stem cells (MSCs), also known as mesenchymal stromal cells, are multipotent stromal cells, and have gained increasing attention due to their wound‑healing ability, as well as their tumor‑promoting potential. MSCs are essential components of the tumor microenvironment and serve important roles in tumor initiation, progression and metastasis. The present review focuses on GC and discusses recent advances in understanding the effect of GC‑derived MSC‑like cells (GC‑MSCs) on tumor progression, chemoresistance and immune escape. Additionally, the mechanism underlying the tumor tropism of bone marrow‑derived MSCs and the malignant transition of these cells to GC‑MSCs are addressed. The potential of GC‑MSCs in the treatment of GC, such as for predicting prognosis and as therapeutic targets, is also discussed in association with their critical role in tumor progression. The information on the characteristics and functions of GC‑MSCs provided in the present review may promote the development of novel therapeutic strategies against GC.