title: Upregulation of extracellular matrix metalloproteinase inducer promotes hypoxia-induced epithelial-mesenchymal transition in esophageal cancer.
abstract: Extracellular matrix metalloproteinase inducer (EMMPRIN) exerts important roles in tumor progression, including angiogenesis, metastasis and therapy resistance. The epithelial‑mesenchymal transition (EMT), which is induced by hypoxia, is an important process in cancer metastasis. However, the association between hypoxia and EMMPRIN remains to be elucidated in esophageal cancer. The expression of EMMPRIN was determined by western blotting and reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), and EMT markers were analyzed by western blotting, RT‑qPCR and immunofluoresence. The migration and invasion of cells was investigated by Transwell assay. The results indicated that the expression levels of EMMPRIN in esophageal cancer cells were markedly higher compared with those in normal esophageal cells. EMMPRIN was able to promote esophageal cancer cell migration and invasion under both hypoxic or normoxic conditions, as demonstrated by the migration and invasion assay. The expression levels of E‑cadherin were reduced, and those of snail family zinc finger 1, fibronectin, α‑smooth muscle actin and fibroblast secretory protein 1 increased in esophageal cancer cells following treatment with human recombinant EMMPRIN under hypoxic conditions. The mRNA expression levels of the EMT markers were similar to those of the protein expression levels. Furthermore, the results demonstrated that EMMPRIN was regulated by hypoxia‑inducible factor (HIF)‑1α. These data suggested that EMMPRIN promoted metastasis and the EMT in esophageal cancer cells by regulating HIF-1α.
authors.affiliation: Department of Oncology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
authors.forename: Xiaopeng
authors.initials: X
authors.lastname: Wu
authors.affiliation: Department of Oncology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
authors.forename: Bin
authors.initials: B
authors.lastname: Qiao
authors.affiliation: Department of Oncology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
authors.forename: Qin
authors.initials: Q
authors.lastname: Liu
authors.affiliation: Department of Oncology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
authors.forename: Weiguo
authors.initials: W
authors.lastname: Zhang
mesh_terms: D051926:Basigin / Q000235:genetics / Q000378:metabolism*; D045744:Cell Line, Tumor; D058750:Epithelial-Mesenchymal Transition; D004938:Esophageal Neoplasms / Q000150:complications / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D004947:Esophagus / Q000473:pathology*; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D000860:Hypoxia / Q000150:complications / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism*; D009362:Neoplasm Metastasis / Q000235:genetics / Q000473:pathology; D015854:Up-Regulation
chemical_list: D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D051926:Basigin