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As the first barrier to the outside environment, airway epithelial cells serve a central role in the initiation and development of airway inflammation. Chemokines are the most direct and immediate cell factors for the recruitment and migration of inflammatory cells. The present review focused on the role of epithelial chemokines in the pathogenesis of airway inflammation in asthma. In addition to traditional CC family chemokines and CXC family chemokines, airway epithelial cells also express other chemokines, including thymic stromal lymphopoietin and interleukin‑33. By expressing and secreting chemokines, airway epithelial cells serve a key role in orchestrating airway inflammation in asthma.

The present study investigated the role of microRNA (miR)‑138‑5p in regulating carcinoma migration and sensitivity to chemotherapy in pancreatic cancer. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was used to assess the expression levels of miR‑138‑5p in pancreatic cancer cell lines and primary carcinoma tissues from human patients. A lentiviral vector, containing miR‑138‑5p mimics (lv‑miR‑138‑m) or miR‑138‑5p inhibitor (lv‑miR‑138‑i), was used to either upregulate or downregulate the expression levels of miR‑138‑5p in PANC‑1 cells, respectively. The effects of miR‑138‑3p regulation on pancreatic cancer cell migration and sensitivity to chemotherapy were examined. The predicted targeting of miR‑138‑5p on vimentin (VIM) was assessed by western blotting in PANC‑1 cells. VIM was subsequently downregulated using small interfering (si)RNA to determine its effect on miR‑138‑5p‑modulated pancreatic cancer cell development. The expression levels of miR‑138‑5p were downregulated in pancreatic cancer cell lines and primary carcinoma tissues. In PANC‑1 cells, lentivirus-mediated upregulation of miR‑138‑5p inhibited cancer cell migration and increased cell chemosensitivity to 5‑fluorouracil (5‑FU). By contrast, downregulation of miR‑138‑5p promoted cancer cell migration and decreased cell chemosensitivity to 5‑FU. A luciferase assay revealed that VIM was a direct target of miR‑138‑5p. Western blotting demonstrated that VIM was downregulated upon the upregulation of miR‑138‑5p in PANC‑1 cells. siRNA‑mediated downregulation of VIM inhibited pancreatic cancer cell migration in the control and miR‑138‑5p downregulated PANC‑1 cells. The present study demonstrated that miR‑138‑5p is important in regulating pancreatic cancer development, possibly through targeting VIM.