Accession Number : ADA328809
Title : Special Distribution of the EGF Receptor System in the Regulation of Breast Epithelia Cell Growth and Organization.
Descriptive Note : Annual rept. 15 May 96-14 May 97,
Corporate Author : UTAH UNIV SALT LAKE CITY
Personal Author(s) : Burke, Patrick M.
PDF Url : ADA328809
Report Date : JUN 1997
Pagination or Media Count : 25
Abstract : 184A1 human mammary epithelial cells (HMECs) form organotypic structures when plated on Matrigel; however, after three weeks on matrigel 184a1 cells do not form polarized, glandular epithelial structures, nor do they polarize if plated onto Transwell tissue culture inserts. Therefore, 184A1 can not be used to address the primary aim of my proposal: to determine if the loss of the correct spatial organization or inappropriate expression of the EGF-R system provides a growth advantage, enhances motility, or changes the differentiated state of normal cells. HB2 cells are a normal, non-transformed mammary epithelial cell line that expresses high numbers of EGF-R, are tightly adherent to transwells, and polarize on transwells as determined by immunofluorescence localization of ZO- 1, the EGF-R and Beta-1 integrin. However, HB2 cells do not consistently polarize the EGF-R population. Experiments are underway to determine if conditions can be found in which HB2 reproducibly polarize their EGF-R population. HB2 cells may provide an experimental system with which to address the primary of my proposal. Preliminary experiments comparing l84Als and HB2 have revealed two interesting and novel findings: (1) rapid internalization of EGF-R can be uncoupled from the normal negative regulatory process of down-regulation; (2) EGF may induce the dephosphorylation of FAK.
Descriptors : *EPITHELIUM, *CELLS(BIOLOGY), *GROWTH(PHYSIOLOGY), *BREAST CANCER, SPATIAL DISTRIBUTION, HUMANS, STRUCTURES, SENSE ORGANS, RECEPTOR SITES(PHYSIOLOGY), MAMMARY GLANDS, TISSUE CULTURE, PHOSPHORUS TRANSFERASES.
Subject Categories : Biochemistry
Anatomy and Physiology
Medicine and Medical Research
Distribution Statement : APPROVED FOR PUBLIC RELEASE