Differentiation-inducing effects of betamethasone on human glioma cell line U251

Abstract

ABSTRACT. We studied the differentiation-inducing effect of betamethasone 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 kinase (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 percentage 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 T. Jin et al. 7842©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (3): 7841-7849 (2015) 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.

Prenatal Betamethasone interferes with immune system development and alters target cells in autoimmune diabetes

“…Although being aware of the differences between primary β-cells and the NOD-derived NIT-1 cell line, it was not technically feasible to obtain islets of Langerhans from newborn pups. The results demonstrated that betamethasone deteriorated NIT-1 cell viability and arrested cell growth, thus preventing the exponential growth phase, as described in other cell lines 39,40 . This effect fits well with the decrease of C-peptide secretion caused by betamethasone, as indirect biomarker of insulin secretion, and with the described effect of synthetic glucocorticoids in islet β-cells, causing a reversible inhibition of insulin secretion 41 but maintaining insulin synthesis.…”