Hyperglycemia impairs the retinal functions in patients with diabetic retinopathy (DR). Downregulation of long non‑coding RNA growth arrest‑specific transcript 5 (lncRNA GAS5) expression in diabetes affects glucose intake and insulin signaling. Sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2 (SERCA2) mediates the regulation of endoplasmic reticulum (ER) stress and apoptosis in high glucose (HG)‑treated podocytes. Therefore, the present study aimed to investigate the roles of lncRNA GAS5 and SERCA2 in retinal pigment epithelium cells exposed to HG. GAS5 expression levels were detected using reverse transcription‑quantitative PCR. In addition, the expression levels of SERCA2b, ER stress‑related proteins, pro‑inflammatory factors and apoptotic proteins were determined by western blot analysis, ELISA or flow cytometry. The results showed that HG treatment induced ER stress in ARPE‑19 human adult retinal pigment epithelial cells by upregulating the expression levels of phosphorylated (p)‑protein kinase R‑like ER kinase, p‑eukaryotic initiation factor 2α, activating transcription factor 4 and CCAAT/enhancer‑binding protein homologous protein. In addition, HG treatment induced apoptosis by increasing Bax, Bad and caspase 12, and by decreasing Bcl‑2 levels expression levels. Moreover, HG treatment induced inflammation by upregulating tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6 expression. However, GAS5 and SERCA2b overexpression significantly decreased ER stress‑related apoptosis and inflammation, whereas SERCA2b knockdown significantly reversed the inhibitory effect of GAS5 on ER stress, apoptosis and inflammation. The results of the present study indicated that GAS5 may suppress ER stress‑induced apoptosis and inflammation by regulating SERCA2b in HG‑treated cells. These data suggested that GAS5 may serve a vital role in the pathogenesis of DR, and it may be considered a potential target for DR therapy.Long non‑coding RNA (lncRNAs) have been identified to play important roles in multiple human diseases via the regulation of cell proliferation, cell invasion, or cell death. However, little is known about the role of lncRNAs in the process of shifts in the Th17/Treg ratio during the progression of juvenile idiopathic arthritis (JIA). The aim of the present study was to determine the role of lncRNA RP11‑340F14.6 in the shifting of the Th17/Treg ratio in JIA. The distribution of the T cell subgroup was detected by flow cytometry in peripheral blood mononuclear cells from patients with JIA and healthy controls. It was found that the expression of lncRNA RP11‑340F14.6 was upregulated, and to positively correlate with that of retinoic acid‑related orphan receptor gamma t (RORγt), and to negatively correlate with Foxp3 expression in patients with JIA. RP11‑340F14.6 induced the expression of its neighbor, P2X7R. Through a P2X7R‑independent approach, this lncRNA was also found to play a pivotal role in stimulating Th17 differentiation and simultaneously suppressing Treg distribution. Taken together, the findings of the present study demonstrate that RP11‑340F14.6 specifically binds to P2X7R, which results in the continuous activation of P2X7R. Thus, RP11‑340F14.6 may serve as a promising therapeutic target for the treatment of JIA.Supplemental oxygen therapy can be life‑saving for premature infants. Our previous study revealed a defect in the autophagic flux in the lung tissues of neonatal rats with hyperoxia‑induced bronchopulmonary dysplasia (BPD), but the underlying mechanism remains unknown. Moreover, there are few innovative treatments that can completely alter the course of BPD. The present study examined the expression of Syntaxin 17 (STX17), a protein necessary for autophagosome‑lysosome binding, in alveolar type II (AT‑II) epithelial cells of neonatal rats with BPD. Neonatal Sprague‑Dawley rats were randomly exposed to elevated O2 levels [fraction of inspired oxygen (FiO2), 0.8; model group] or normal room air (FiO2, 0.21; control group), and the expression levels of STX17, autophagy‑related [Microtubule‑associated protein 1A/1B‑light chain 3B (LC3B)‑II, p62, lysosomal‑associated membrane protein 1)] and apoptosis‑related (cleaved caspase3) mRNA and proteins were examined in lung tissues. Moreover, the expression levels of theed to hyperoxia. Collectively, these results indicated that STX17 expression in AT‑II cells was reduced in the early stages of BPD in neonatal rats and may be related to the subsequent hyperoxia‑induced block in autophagic flux.Respiratory syncytial virus (RSV) infection enhances the cell‑mediated immune responses of type 2 helper T cells and promotes the progression of allergic inflammation and asthma by producing thymic stromal lymphopoietin (TSLP), especially long isoform TSLP (lfTSLP). However, the role of short isoform TSLP (sfTSLP) in RSV infection remains to be elucidated. The present study was designed to demonstrate the role of both lfTSLP and sfTSLP, as transcription regulators, in RSV infection. The expression of lfTSLP and sfTSLP in RSV‑infected Beas‑2B cells was analyzed. Activating protein 2 (AP‑2)α was overexpressed or knocked down to detect the changes in sfTSLP and lfTSLP expression. Luciferase reporter plasmid and chromatin immunoprecipitation experiments demonstrated that AP‑2α bound to the sfTSLP promoter region. LfTSLP and sfTSLP increased while AP‑2α decreased in RSV‑infected Beas‑2B cells. In the Beas‑2B cells, AP‑2α was found to negatively regulate the activity of the sfTSLP promoter and the mRNA level of sfTSLP. AP‑2α also negatively regulated the expression of lfTSLP at both the mRNA and protein levels. The results of the chromatin immunoprecipitation assay indicated that AP‑2α bound to the core promoter region of sfTSLP. These results confirmed that the transcription factor AP‑2α can repress the expression of lfTSLP and sfTSLP in bronchial epithelial cells in RSV infection.Glioblastoma multiforme (GBM) is the most common and malignant brain tumor of the adult central nervous system and is associated with poor prognosis. The present study aimed to identify the hub genes in GBM in order to improve the current understanding of the underlying mechanism of GBM. The RNA‑seq data were downloaded from The Cancer Genome Atlas database. The edgeR package in R software was used to identify differentially expressed genes (DEGs) between two groups Glioblastoma samples and normal brain samples. Gene Ontology (GO) functional enrichment analysis and the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis were performed using Database for Annotation, Visualization and Integrated Discovery software. Additionally, Cytoscape and Search Tool for the Retrieval of Interacting Genes/Proteins tools were used for the protein‑protein interaction network, while the highly connected modules were extracted from this network using the Minimal Common Oncology Data Elements plugin. Next, the prognostic significance of the candidate hub genes was analyzed using UALCAN. In addition, the identified hub genes were verified by reverse transcription‑quantitative (RT‑q) PCR. In total, 1,483 DEGs were identified between GBM and control samples, including 954 upregulated genes and 529 downregulated genes (P16) and these genes were involved in different GO terms and signaling pathways. Furthermore, CDK1, BUB1, BUB1B, CENPA and GNG3 were identified as key genes in the GBM samples. The UALCAN tool verified that higher expression level of CENPA was relevant to poorer overall survival rates. In conclusion, CDK1, BUB1, BUB1B, CENPA and GNG3 were found to be potential biomarkers for GBM. Additionally, ‚cell cycle‘ and ‚γ‑aminobutyric acid signaling‘ pathways may serve a significant role in the pathogenesis of GBM.Pancreatic ductal adenocarcinoma (PDAC) is a highly malignant cancer of the digestive tract that has a high potential for metastasis and a poor prognosis. Girdin was first reported in 2005 as an actin‑binding protein and was designated as Akt‑phosphorylation enhancer (APE); thus, Girdin has been revealed to have an important role in regulating cancer development. There is additional evidence indicating that Girdin is associated with cell proliferation, migration, invasion and survival in certain cancers. However, the potential mechanisms involving Girdin and mobility in pancreatic cancer have not been elucidated. In the present study, it was revealed that Girdin was highly expressed in pancreatic cancer tissue and was associated with tumor grade. The present study, to the best of our knowledge, is the first aimed at investigating the unknown role of Girdin in PDAC metastasis. A short hairpin RNA for Girdin (sh‑Girdin) was successfully constructed with recombinant adenoviral vectors to suppress the expression of the interstitial phenotype, decreased in response to sh‑Girdin. According to these experiments, Girdin may affect pancreatic cancer progression and development by interacting with vimentin. Therefore, there is evidence indicating that Girdin could be designated as a prognostic biological indicator and a candidate therapeutic target for pancreatic cancer.Osteosarcoma (OS) has been demonstrated to be difficult to cure due to its potently malignant metastasis. Therefore, new therapeutic approaches blocking the metastatic potential of OS are urgently required to improve the outcomes for OS patients. In the present study, the anti‑metastatic capacity of sea cucumber (Cucumaria frondosa) fucoidan (Cf‑Fuc) was evaluated on osteosarcoma cells by cell adhesion assay, Transwell assay and U2OS cell migration assay. The underlying mechanism on the dynamic remodeling of the cytoskeleton was also explored. The present data indicated that Cf‑Fuc could block the U2OS osteosarcoma cell adhesion to fibronectin and significantly inhibit U2OS cell migration. Cf‑Fuc greatly impaired the migration capacity of U2OS cells, and the migrated distance and velocity of Cf‑Fuc‑treated cells were markedly reduced. Also, Cf‑Fuc could impair the dynamic remodeling of the cytoskeleton possibly by suppressing the phosphorylation of focal adhesion kinase and paxillin, as well as the activation of the Rac1/PAK1/LIMK1/cofilin signaling axis. Collectively, the present findings provide a novel therapeutic potential of C. frondosa fucoidan for osteosarcoma metastasis.Cancer‑associated fibroblasts (CAFs) exhibit tumor‑stimulating properties and are associated with poor survival in several types of cancer, making them potential therapeutic targets. The present study aimed to determine whether CAFs were associated with cell migration and invasion in lung squamous cell carcinoma (LUSC), as well as their association with microRNA‑369 (miR‑369) in these processes. Firstly, the changes of the malignant biological behavior were observed by treating the LUSC cells with the CAFs‑derived extracellular vesicles (CAFs‑EVs). Subsequently, the differentially expressed miRNAs in the cells treated with CAFs‑EVs were analyzed by microarray analysis. Following inhibition of miR‑369 expression in CAFs‑EVs, LUSC cells were co‑cultured, and the malignant biological behavior of the cells was re‑examined. Phlorizin mouse Then, through bioinformatics analysis and verification, the mRNA targets of miR‑369 and the corresponding downstream signaling pathway were screened out. Finally, the effects of CAFs‑EVs on the growth and metastasis of LUSC were demonstrated by in vivo tumor formation and metastasis experiments.