Dexamethasone-induced inhibition of miR-132 via methylation promotes TGF-β-driven progression of pancreatic cancer.

ABSTRACT: Glucocorticoids (GCs) such as dexamethasone (DEX) are administered as cancer co‑treatment for palliative purposes due to their pro‑apoptotic effects in lymphoid cancer and limited side effects associated with cancer growth and chemotherapy. However, there is emerging evidence that GCs induce therapy resistance in most epithelial tumors. Our recent data reveal that DEX promotes the progression of pancreatic ductal adenocarcinoma (PDA). In the present study, we examined 1 primary and 2 established PDA cell lines, and 35 PDA tissues from patients who had received (n=14) or not received (n=21) GCs prior to surgery. Through microRNA microarray analysis, in silico, and RT‑qPCR analyses, we identified 268 microRNAs differentially expressed between DEX‑treated and untreated cells. With a focus on

SUBMITTER: Abukiwan A 

PROVIDER: S-EPMC6255064 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature