To analyze mode-of-action, immune therapies such as trispecific T-cell engagers in leukemia or toxicity on non-cancer cells, the model can be modularly enriched with human endothelial cells (hECs), immune cells and fibroblasts. Upon addition of hECs, transmigration of immune cells through the endothelial barrier can be investigated. In an allogenic CRC model, we observe a lower basic apoptosis rate after applying PBMCs in 3D compared to 2D, which offers new options to mirror antigen-specific immunotherapies in vitro. In conclusion, we present modular human 3D tumor models with tissue-like features for preclinical testing to reduce animal experiments.Bone loss is a disease that is highly associated with aging. This deleterious health condition has become a public concern worldwide, and there is an urgent need to discover more novel therapeutic strategies for the development of age‑associated osteoporosis. The present study aimed to explore the association between proprotein convertase subtilisin/kexin type 5 (PCSK5) and microRNA(miR)‑338‑3p in bone‑formation and bone‑loss processes. Western blotting assay and reverse transcription‑quantitative PCR were employed to analyze PCSK5 and miR‑338‑3p expression levels in bone mesenchymal stem cells (BMSCs). Dual‑luciferase reporter and RNA pull‑down assays were used to determine the target. For osteoblastic differentiation verification, alkaline phosphatase activity, osteocalcin secretion detection, bone formation‑related indicators (osterix, runt‑related gene 2, osteopontin and bone sialoprotein), hematoxylin and eosin staining and Alizarin Red S staining were performed. The findings of the present study indicated that the expression level of PCSK5 was higher in BMSCs from young rat samples, whereas the expression level of miR‑338‑3p was higher in BMSCs from samples of old rats. Experimental results also revealed that unlike miR‑338‑3p, downregulation of PCSK5 inhibited osteoblastic differentiation and osteogenesis by inhibiting alkaline phosphatase, osteocalcin, osterix, runt‑related transcription factor 2, osteopontin, bone sialoprotein and mineralized nodule formation. Overall, the results suggested that miR‑338‑3p could suppress age‑associated osteoporosis by regulating PCSK5.Dendritic cells release bioactive exosomes involved in immune regulation. Long non‑coding RNAs (lncRNAs) are implicated in a number of immunoregulatory mechanisms. However, the roles of lncRNAs in dendritic cell‑derived exosomes remain to be elucidated. The present study aimed to investigate the roles of lncRNAs in exosomes derived from mature and immature dendritic cells and to find specific lncRNAs with immunoregulatory function. The expression profiles of lncRNAs in exosomes derived from bone marrow dendritic cells of C57 mice were illustrated. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses and Gene Set Enrichment Analysis were performed to identify potential targets correlated with immune regulation. In addition, lncRNA‑miRNA‑mRNA networks were predicted using bioinformatics methods. Representative lncRNAs were further validated via reverse transcription‑quantitative PCR. A total of 437 lncRNAs were analyzed using RNA‑seq. Among these, the expression of ~87 lncRNAs was upregulated and 21 lncRNAs was downregulated in mature dendritic cell‑derived exosomes (Dex) compared with immature Dex. GO analyses indicated the involvement of upregulated lncRNAs in multiple biological functions, such as the immune system process, while downregulated lncRNAs were involved in poly(A) RNA binding. Analysis of the KEGG pathway identified the relationship of TNF signaling and ribosome pathway with upregulated lncRNAs and downregulated lncRNAs, respectively. The results of gene set enrichment analysis identified that three lncRNA‑associated transcripts (Procr‑203, Clec4e‑202 and Traf1‑203) were highly associated with immunoregulatory functions including T helper cell differentiation and Janus kinase‑STAT signaling pathway. The results indicated the involvement of candidate lncRNAs in immunoregulation and suggested a new perspective on the modulation of lncRNAs in Dex.Radioresistance is the primary roadblock limiting the success of treatment of nasopharyngeal carcinoma (NPC). microRNA (miRNA/miR)‑182‑5p has been reported to affect the sensitivity of cancer cells to irradiation; however, the role of miR‑182‑5p in NPC has not been assessed. The aim of the present study was to investigate the contribution of miR‑182‑5p to the radioresistance of NPC cells. The key mRNA and miRNA involved in NPC radioresistance were identified using bioinformatics analysis. The two cell lines used in the present study were 5‑8F cells (radio‑sensitive) and 5‑8F‑R cells (radioresistant). A dual‑luciferase reporter assay system was used to validate the binding between BCL2/adenovirus E1B 19 kDa protein‑interacting protein 3 (BNIP3) mRNA and miR‑182‑5p. Reverse transcription‑quantitative PCR and western blotting were used to determine the RNA and protein expression levels. To obtain a deeper insight into the effects of the BNIP3/miR‑182‑5p axis on NPC radioresistance, Cell Counting Kit‑8, wound healing, Transwell invasion and colony formation assays, as well as flow cytometry analysis were performed. The results showed that miR‑182‑5p and BNIP3 were up and downregulated, respectively, in 5‑8F‑R cells. BNIP3 was also confirmed to be the target of miR‑182‑5p, and miR‑182‑5p reversed the inhibitory effect of BNIP3 in 5‑8F‑R cells. The cellular experiments showed that upregulation of BNIP3 not only inhibited cell proliferation, viability, invasion and migration, but also promoted the apoptosis of 5‑8F‑R cells.  https://www.selleckchem.com/products/ipi-549.html  However, the effects of BNIP3 were attenuated by the simultaneous upregulation of miR‑182‑5p. Thus, through downregulation of BNIP3, miR‑182‑5p contributed to radiation resistance of NPC cells.Lung cancer is the most common cancer type worldwide and the leading cause of cancer-related mortality. Diabetes is closely associated with the occurrence, development and prognosis of lung cancer. Therefore, the present study aimed to investigate whether SNCG could affect the proliferation of lung cancer cells induced by high glucose. Lung cancer cells induced by high glucose simulated the pathologies of patients with lung cancer with diabetes in vitro. The proliferation of HBE cells and lung cancer cells after transfection and treatment of glucose was detected using Cell Counting Kit-8 assay. The mRNA expression levels of synuclein γ (SNCG), insulin-like growth factor 1 (IGF-1) and IGF-1 receptor (IGF-1R) in HBE cells and lung cancer cells alone, or cells induced by high glucose were analyzed via reverse transcription-quantitative (RT-q)PCR analysis. Moreover RT-qPCR analysis was used to determine the transfection efficiencies. The clone formation ability, migration and inflammation of lung cancer cells after high glucose induction and transfection were detected using clone formation, wound healing and ELISA assays.