Retinoic acid (RA) inhibits growth, increases the cytokeratin content, and alters the cytoskeleton of the human cervical cell line NHIK 3025. Using RA-treated NHIK 3025 cells as immunogen we prepared murine monoclonal antibodies (IgG1) which recognized an RA-induced cell-surface antigen which could not be detected in untreated NHIK 3025 cells. Analysis of the Triton soluble proteins by SDS-gel electrophoresis and immunoblotting revealed that the cell-surface antigen is a 140-kDa glycoprotein (gp140). gp140 was also shown to be induced by RA in HeLa S3 cells and constitutively expressed in the human trophoblast cell line BeWo. gp140 was also detected in other human epithelial cell lines, but not in human hematopoietic cells. Expression of gp140 was induced in HeLa S3 cells by nanomolar concentrations of RA, and in NHIK 3025 cells by micromolar amounts (1-10 microM). The glycoprotein was detectable 3-6 h following exposure to RA and its expression was reversible upon removal of RA from the medium. Our results indicate that gp140 is a newly identified RA-inducible epithelial membrane glycoprotein which may represent a phenotypic differentiation marker for epithelial cells.
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http://dx.doi.org/10.1016/0014-4827(89)90208-5 | DOI Listing |
Tissue Eng Part A
February 2014
1 FMC BioPolymer AS/NovaMatrix , Sandvika, Norway .
Essential cellular functions are often lost under culture in traditional two-dimensional (2D) systems. Therefore, biologically more realistic three-dimensional (3D) cell culture systems are needed that provide mechanical and biochemical cues which may otherwise be unavailable in 2D. For the present study, an alginate-based hydrogel system was used in which cells in an alginate solution were seeded onto dried alginate foams.
View Article and Find Full Text PDFJ Radiat Res
November 2013
Department of Physics, University of Oslo, 0316 Oslo, Norway.
In this study, a mechanism in which low-dose hyper-radiosensitivity (HRS) is permanently removed, induced by low-dose-rate (LDR) (0.2-0.3 Gy/h for 1 h) but not by high-dose-rate priming (0.
View Article and Find Full Text PDFActa Oncol
September 2007
Department of Medical Physics, The University of Oslo, Oslo, Norway.
The iso-effective irradiation of continuous low-dose-rate (CLDR) irradiation was compared with that of various schedules of pulsed dose rate (PDR) irradiation for cells of two established human lines, T-47D and NHIK 3025. Complete single-dose response curves were obtained for determination of parameters alpha and beta by fitting of the linear quadratic formula. Sublethal damage repair constants micro and T(1/2) were determined by split-dose recovery experiments.
View Article and Find Full Text PDFAnticancer Res
November 2005
Department of Physics, The Biophysics Group, University of Oslo, P.O. Box 1048 Blindern, 0316 Oslo, Norway.
We have studied hypoxia-induced cell cycle arrest in human cells where the retinoblastoma tumour suppressor protein (pRb) is either functional (T-47D cells) or abrogated by expression of the HPV18 E7 oncoprotein (NHIK 3025 cells). Cells of both types are arrested in a restriction point in late G1, here denoted as the oxygen-dependent restriction point in late G1. This arrest seems to occur under extreme hypoxia in all types of mammalian cells so far tested.
View Article and Find Full Text PDFCell Prolif
October 2004
Department of Physics, The Biophysics Group, The University of Oslo, Oslo, Norway.
We have studied hypoxia-induced cell cycle arrest in human cells where the retinoblastoma tumour suppressor protein (pRb) is either functional (T-47D and T-47DHU-res cells) or abrogated by expression of the HPV18 E7 oncoprotein (NHIK 3025 cells). We have previously found that pRb is dephosphorylated and rebound in the nucleus in T-47D cells arrested in S-phase during hypoxia and that this binding is protracted even following re-oxygenation. In the present study, however, we show that the long-lasting arrest following re-oxygenation induced by pRb-binding in the cell nuclei may be overruled by an elevated level of ribonucleotide reductase (RNR).
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