title: Differentiation-inducing effects of betamethasone on human glioma cell line U251.
abstract: We studied the differentiation-inducing effect of beta-methasone on human glioma cell line U251 cultured in vitro, and the underlying mechanism. U251 cells were divided into two groups: control group cells, cultured in Dulbecco's Modified Eagle's medium containing 10% fetal bovine serum; and medication group cells, treated with 15 μM betamethasone. Morphological cell changes were observed by inverted microscope, cell cycle changes were ascertained by flow cytometry, and vimentin expression was checked by immunocytochemistry. The expression levels of extracellular signal-regulated protein ki-nase (ERK), phosphorylated ERK (pERK), and glial fibrillary acidic protein (GFAP) were assessed by western blot. Compared with the control group, U251 cell processes increased significantly, but declined 96 h after betamethasone took effect. After 48 h, the percentage of S-phase cells decreased significantly (28.77 to 20.42%; P = 0.014); the percent-age of strongly positive vimentin cells decreased significantly (91 to 51%; P = 0.0092); and the ratio of expression of GFAP protein to the internal control β-actin increased significantly (0.24 to 0.53; P = 0.1). The level of ERK protein did not change significantly 48 and 96 h after the action of betamethasone, and the pERK/ERK ratios were 0.37 and 0.23, respectively, which were significantly reduced compared with the control group (P = 0.028 and 0.006). Betamethasone has a significant effect on the induction and differentiation of U251 cells, and its mechanism may be related to the inhibition of the abnormal activation of the ERK signal pathway.
authors.affiliation: The First Affiliated Hospital of Liaoning Medical University, Jinzhou, China.
authors.forename: T
authors.initials: T
authors.lastname: Jin
authors.affiliation: Department of Neurology, The First Affiliated Hospital of Dalian Medical University, Dalian, China.
authors.forename: Y X
authors.initials: YX
authors.lastname: Wang
authors.affiliation: Department of Anatomy, Dalian Medical University, Dalian, China.
authors.forename: K
authors.initials: K
authors.lastname: Fan
authors.affiliation: Department of Neurology, The First Affiliated Hospital of Dalian Medical University, Dalian, China.
authors.forename: D B
authors.initials: DB
authors.lastname: Tao
authors.affiliation: Department of Neurology, The First Affiliated Hospital of Dalian Medical University, Dalian, China.
authors.forename: X
authors.initials: X
authors.lastname: Dong
authors.affiliation: Department of Neurology, The First Affiliated Hospital of Dalian Medical University, Dalian, China.
authors.forename: J S
authors.initials: JS
authors.lastname: Shen
mesh_terms: D001623:Betamethasone / Q000494:pharmacology*; D001932:Brain Neoplasms / Q000378:metabolism / Q000473:pathology*; D002453:Cell Cycle / Q000187:drug effects; D002454:Cell Differentiation / Q000187:drug effects*; D045744:Cell Line, Tumor; D048430:Cell Shape / Q000187:drug effects; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005910:Glioma / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D010766:Phosphorylation / Q000187:drug effects; D014746:Vimentin / Q000378:metabolism
chemical_list: D005904:Glial Fibrillary Acidic Protein; D014746:Vimentin; D001623:Betamethasone; D048049:Extracellular Signal-Regulated MAP Kinases