Radiation Induced Apoptosis of Murine Bone Marrow Cells Is Independent of Early Growth Response 1 (EGR1)

Autor: Ying Liang, Mary K. McKenna, Vivek M. Rangnekar, Daret K. St. Clair, Karine Z. Oben, Beth W. Gachuki, Subbarao Bondada, Sara S. Alhakeem
Jazyk: angličtina
Rok vydání: 2017
Předmět:
0301 basic medicine
Myeloid
Carcinogenesis
Cell
Cancer Treatment
lcsh:Medicine
Apoptosis
Suppressor Genes
Malignant transformation
Histones
Mice
Animal Cells
Radiation
Ionizing
Medicine and Health Sciences
Transcriptional regulation
DNA Breaks
Double-Stranded
lcsh:Science
Cells
Cultured
Staining
education.field_of_study
Radiation
Multidisciplinary
Cell Death
Physics
Stem Cells
Cell Staining
Hematopoietic stem cell
Up-Regulation
3. Good health
medicine.anatomical_structure
Oncology
Cell Processes
Physical Sciences
Cellular Types
Whole-Body Irradiation
Neoplastic Transformation
Research Article
endocrine system
Tumor Suppressor Genes
Population
Bone Marrow Cells
Biology
Real-Time Polymerase Chain Reaction
Research and Analysis Methods
03 medical and health sciences
Gene Types
Genetics
medicine
Animals
RNA
Messenger
education
Early Growth Response Protein 1
Nuclear Physics
Tibia
lcsh:R
Biology and Life Sciences
Cell Biology
Hematopoietic Stem Cells
030104 developmental biology
Microscopy
Fluorescence
Specimen Preparation and Treatment
Ionizing Radiation
Cancer research
lcsh:Q
Bone marrow
Tumor Suppressor Protein p53
Zdroj: PLoS ONE, Vol 12, Iss 1, p e0169767 (2017)
PLoS ONE
ISSN: 1932-6203
Popis: An understanding of how each individual 5q chromosome critical deleted region (CDR) gene contributes to malignant transformation would foster the development of much needed targeted therapies for the treatment of therapy related myeloid neoplasms (t-MNs). Early Growth Response 1 (EGR1) is a key transcriptional regulator of myeloid differentiation located within the 5q chromosome CDR that has been shown to regulate HSC (hematopoietic stem cell) quiescence as well as the master regulator of apoptosis—p53. Since resistance to apoptosis is a hallmark of malignant transformation, we investigated the role of EGR1 in apoptosis of bone marrow cells; a cell population from which myeloid malignancies arise. We evaluated radiation induced apoptosis of Egr1+/+ and Egr1-/- bone marrow cells in vitro and in vivo. EGR1 is not required for radiation induced apoptosis of murine bone marrow cells. Neither p53 mRNA (messenger RNA) nor protein expression is regulated by EGR1 in these cells. Radiation induced apoptosis of bone marrow cells by double strand DNA breaks induced p53 activation. These results suggest EGR1 dependent signaling mechanisms do not contribute to aberrant apoptosis of malignant cells in myeloid malignancies.
Databáze: OpenAIRE
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