title: Activation of NFkB is a novel mechanism of pro-survival activity of glucocorticoids in breast cancer cells.
abstract: Glucocorticoids (GCs) are pro-apoptotic as a co-medication to treat leukemia and lymphoma. However, the effects in breast cancer (BC) are diverse with mechanisms less understood. In this study using BC model cell MCF7, we found that dexamethasone (Dex) promotes cell proliferation. Gene expression analysis identified that c-Myc was enhanced by Dex, providing an important link to the pro-survival effect of GCs in BC. Dex treatment promoted NFkB transcriptional activity leading to the up-regulation of c-Myc. RelA was activated by Dex but with decreased interaction with GR, thus identifying a new pattern of regulation of NFkB by GC/GR in BC cells.
authors.affiliation: Department of Basic Sciences, The Commonwealth Medical College, Scranton, PA 18509, USA.
authors.forename: Shagufta
authors.initials: S
authors.lastname: Khan
authors.forename: Zenaida
authors.initials: Z
authors.lastname: Lopez-Dee
authors.forename: Raj
authors.initials: R
authors.lastname: Kumar
authors.forename: Jun
authors.initials: J
authors.lastname: Ling
mesh_terms: D001943:Breast Neoplasms / Q000378:metabolism / Q000473:pathology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D003907:Dexamethasone / Q000494:pharmacology*; D005260:Female; D006801:Humans; D016328:NF-kappa B / Q000378:metabolism*; D016271:Proto-Oncogene Proteins c-myc / Q000096:biosynthesis; D011965:Receptors, Glucocorticoid / Q000502:physiology; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: C489427:MYC protein, human; D016328:NF-kappa B; D016271:Proto-Oncogene Proteins c-myc; C498143:RELA protein, human; D011965:Receptors, Glucocorticoid; D051996:Transcription Factor RelA; D003907:Dexamethasone
keywords: Breast cancer; Glucocorticoid receptor (GR); NFkB; c-Myc