title: Concurrent down-regulation of Egr-1 and gelsolin in the majority of human breast cancer cells.
abstract: A growing body of evidence suggests that early growth response-1 (Egr-1), a transcription factor, may function as a tumor suppressor. The aim of this study was to gain more evidence to support the role of Egr-1 in the suppression of cancer cell growth and to examine the potential correlation between Egr-1 and gelsolin.
  
  
  METHODS
  Histochemical staining coupled with breast cancer tissue arrays were used to examine the expression levels of Egr-1 and gelsolin. Reporter assays and gel shift were used to study the transcriptional activity of Egr-1 on the regulation of gelsolin.
  
  
  RESULTS
  Our data showed that most normal mammary tissues expressed high levels of Egr-1, while the majority of breast cancer tissues expressed very small amounts of Egr-1. The expression pattern of Egr-1 in human breast cancer tissues was highly correlated with gelsolin expression. Induction of Egr-1 by serum stimulation accompanied the increase of gelsolin expression. In cells lacking the induction of Egr-1 in response to serum stimulation, gelsolin expression remained unchanged. Furthermore, gelsolin promoter activity was profoundly reduced in Egr-1 null mouse embryonic fibroblasts compared to Egr-1 wild-type mouse embryonic fibroblasts. Gel shift experiments indicated that Egr-1 can directly bind to the gelsolin promoter.
  
  
  CONCLUSIONS
  Our results suggest that Egr-1 may be an important breast cancer marker and that an as yet uncharacterized pathway involved in Egr-1 and gelsolin expression exists which leads to breast cancer cell development.
authors.affiliation: Department of Gynecology and Obstetrics, Emory University School of Medicine, Atlanta, GA 30322, USA.
authors.forename: Jingbo
authors.initials: J
authors.lastname: Liu
authors.forename: Ya-Guang
authors.initials: YG
authors.lastname: Liu
authors.forename: Ruochun
authors.initials: R
authors.lastname: Huang
authors.forename: Chen
authors.initials: C
authors.lastname: Yao
authors.forename: Shiyong
authors.initials: S
authors.lastname: Li
authors.forename: Weimin
authors.initials: W
authors.lastname: Yang
authors.forename: Dongzi
authors.initials: D
authors.lastname: Yang
authors.forename: Ruo-Pan
authors.initials: RP
authors.lastname: Huang
mesh_terms: D000818:Animals; D001665:Binding Sites; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D045744:Cell Line, Tumor; D015536:Down-Regulation; D051766:Early Growth Response Protein 1 / Q000235:genetics* / Q000378:metabolism*; D018260:Gelsolin / Q000235:genetics* / Q000378:metabolism*; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D051379:Mice; D011401:Promoter Regions, Genetic / Q000235:genetics; D013997:Time Factors
chemical_list: C497325:EGR1 protein, human; D051766:Early Growth Response Protein 1; D018260:Gelsolin