scholarly journals Human telomerase is regulated by erythropoietin and transforming growth factor-β in human erythroid progenitor cells

Leukemia ◽  
2007 ◽  
Vol 21 (11) ◽  
pp. 2304-2310 ◽  
Author(s):  
N Prade-Houdellier ◽  
E Frébet ◽  
C Demur ◽  
E-F Gautier ◽  
F Delhommeau ◽  
...  
Keyword(s):  
Growth Factor ◽  
Progenitor Cells ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Erythroid Progenitor ◽  
Erythroid Progenitor Cells ◽  
Human Telomerase

scholarly journals The Raf‐1 Protein Mediates Insulin‐Like Growth Factor‐Induced Proliferation of Erythroid Progenitor Cells

Stem Cells ◽  
1998 ◽  
Vol 16 (3) ◽  
pp. 200-207 ◽  
Author(s):  
Marilyn R. Sanders ◽  
Hsienwie Lu ◽  
Frederick Walker ◽  
Sandra Sorba ◽  
Nicholas Dainiak
Keyword(s):  
Growth Factor ◽  
Progenitor Cells ◽  
Erythroid Progenitor ◽  
Erythroid Progenitor Cells

scholarly journals Tumor Immune Evasion Induced by Dysregulation of Erythroid Progenitor Cells Development

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 870
Author(s):  
Tomasz M. Grzywa ◽  
Magdalena Justyniarska ◽  
Dominika Nowis ◽  
Jakub Golab
Keyword(s):  
T Cells ◽  
Tumor Growth ◽  
Progenitor Cells ◽  
Cancer Progression ◽  
Immune Evasion ◽  
Transforming Growth Factor ◽  
Early Stage ◽  
Interleukin 10 ◽  
Erythroid Progenitor ◽  
Erythroid Progenitor Cells

Cancer cells harness normal cells to facilitate tumor growth and metastasis. Within this complex network of interactions, the establishment and maintenance of immune evasion mechanisms are crucial for cancer progression. The escape from the immune surveillance results from multiple independent mechanisms. Recent studies revealed that besides well-described myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs) or regulatory T-cells (Tregs), erythroid progenitor cells (EPCs) play an important role in the regulation of immune response and tumor progression. EPCs are immature erythroid cells that differentiate into oxygen-transporting red blood cells. They expand in the extramedullary sites, including the spleen, as well as infiltrate tumors. EPCs in cancer produce reactive oxygen species (ROS), transforming growth factor β (TGF-β), interleukin-10 (IL-10) and express programmed death-ligand 1 (PD-L1) and potently suppress T-cells. Thus, EPCs regulate antitumor, antiviral, and antimicrobial immunity, leading to immune suppression. Moreover, EPCs promote tumor growth by the secretion of growth factors, including artemin. The expansion of EPCs in cancer is an effect of the dysregulation of erythropoiesis, leading to the differentiation arrest and enrichment of early-stage EPCs. Therefore, anemia treatment, targeting ineffective erythropoiesis, and the promotion of EPC differentiation are promising strategies to reduce cancer-induced immunosuppression and the tumor-promoting effects of EPCs.

Two forms of transforming growth factor-β distinguished by multipotential haematopoietic progenitor cells

Nature ◽  
1987 ◽  
Vol 329 (6139) ◽  
pp. 539-541 ◽  
Author(s):  
Masatsugu Ohta ◽  
Joel S. Greenberger ◽  
Pervin Anklesaria ◽  
Anna Bassols ◽  
Joan Massagué
Keyword(s):  
Growth Factor ◽  
Progenitor Cells ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β

Insulin-Like Growth Factor II Is an Autocrine Growth Factor To Prevent Apoptosis as Well as To Enhance Proliferation and Maturation of Erythroid Progenitor Cells.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3140-3140
Author(s):  
Taro Nagatomo ◽  
Koichiro Muta ◽  
Shouichi Ohga ◽  
Masayuki Ochiai ◽  
Shunji Hikino ◽  
...  
Keyword(s):  
Growth Factor ◽  
Progenitor Cells ◽  
Liquid Culture ◽  
Neutralizing Antibody ◽  
Vascular Endothelial ◽  
Insulin Like Growth Factor ◽  
Erythroid Progenitor ◽  
Erythroid Progenitor Cells ◽  
Factor Ii ◽  
Endothelial Growth Factor

Abstract To reveal the novel function of erythroid progenitor cells in fetal erythropoiesis, the gene expression pattern in umbilical cord blood (CB)-derived CD36+ erythroid progenitor cells (EPCs) was analyzed using cDNA microarray containing 240 cytokine and growth factor related genes. Among the genes analyzed, insulin-like growth factor II (IGF-II) gene showed a 124-fold higher level of expression in CB-EPCs, compared with that seen in phytohemagglutinin (PHA)-stimulated adult peripheral blood mononuclear cells (PBMCs) (table1). Real-time PCR revealed that the IGF-II mRNA levels in CB-EPCs were higher than those seen in lymphocytes or monocytes separated from CB or PBMCs. When CB-EPCs were cultured with erythropoietin (EPO) in serum-free medium, the number of erythroid colonies was decreased in the presence of IGF-II-neutralizing antibody. To further assess the role of IGF-II in erythropoiesis, we purified erythroid colony-forming cells (ECFCs) from human umbilical cord blood by magnetic selection and liquid culture with IL-3, stem cell factor and EPO. The expression levels of IGF-II, type 1 or 2 IGF receptor in the mature ECFCs were higher than those in the immature ECFCs. Addition of IGF-II-neutralizing antibody decreased the number of ECFCs in liquid culture with EPO. The anti-proliferative effect of IGF-II-neutralizing antibody was evident in both dimethylthiazole tetrazolium bromide (MTT) and bromodeoxyuridine (BrdU) incorporation assays. When apoptosis of cells was examined using Annexin V, the addition of IGF-II-neutralizing antibody increased apoptosis, thereby indicating the anti-apoptotic effects of IGF-II secreted from erythroid cells. Furthermore, ECFCs failed to undergo normal erythroid maturation in the presence of IGF-II-neutralizing antibody, as assessed by flow cytometric and morphologic analyses. These findings indicate that IGF-II, which is produced by erythroid progenitor cells themselves, has crucial roles in controlling erythropoiesis by modulating apoptosis, proliferation and maturation via an autocrine mechanism. Cytokine and growth factor genes highly expressed in CB-EPCs selected by cDNA microarray analyses ratio gene 124.0 insulin-like growth factor II 7.9 vascular endothelial growth factor 3.9 interleukin 8 3.4 GRO2 oncogene 3.0 GRO1 oncogene 1.6 transforming growth factor, beta 1 1.4 vascular endothelial growth factor B

scholarly journals BF-1 Interferes with Transforming Growth Factor β Signaling by Associating with Smad Partners

2000 ◽  
Vol 20 (17) ◽  
pp. 6201-6211 ◽  
Author(s):  
Changlin Dou ◽  
Jun Lee ◽  
Bo Liu ◽  
Fang Liu ◽  
Joan Massague ◽  
...  
Keyword(s):  
Growth Factor ◽  
Dna Binding ◽  
Growth Inhibition ◽  
Progenitor Cells ◽  
Transcriptional Activation ◽  
Transforming Growth Factor ◽  
Ectopic Expression ◽  
Transforming Growth Factor Β ◽  
Reporter System ◽  
Transcriptional Responses

ABSTRACT The winged-helix (WH) BF-1 gene, which encodes brain factor 1 (BF-1) (also known as foxg1), is essential for the proliferation of the progenitor cells of the cerebral cortex. Here we show that BF-1-deficient telencephalic progenitor cells are more apt to leave the cell cycle in response to transforming growth factor β (TGF-β) and activin. We found that ectopic expression of BF-1 in vitro inhibits TGF-β mediated growth inhibition and transcriptional activation. Surprisingly, we found that the ability of BF-1 to function as a TGF-β antagonist does not require its DNA binding activity. Therefore, we investigated whether BF-1 can inhibit Smad-dependent transcriptional responses by interacting with Smads or Smad binding partners. We found that BF-1 does not interact with Smads. Because the identities of the Smad partners mediating growth inhibition by TGF-β are not clearly established, we examined a model reporter system which is known to be activated by activin and TGF-β through Smads and the WH factor FAST-2. We demonstrate that BF-1 associates with FAST-2. This interaction is dependent on the same region of protein which mediates its ability to interfere with the antiproliferative activity of TGF-β and with TGF-β-dependent transcriptional activation. Furthermore, the interaction of FAST-2 with BF-1 is mediated by the same domain which is required for FAST-2 to interact with Smad2. We propose a model in which BF-1 interferes with transcriptional responses to TGF-β by interacting with FAST-2 or with other DNA binding proteins which function as Smad2 partners and which have a common mode of interaction with Smad2.

scholarly journals The roles of transforming growth factor-β, Wnt, Notch and hypoxia on liver progenitor cells in primary liver tumours

2014 ◽  
Vol 44 (4) ◽  
pp. 1015-1022 ◽  
Author(s):  
ELIENE BOGAERTS ◽  
FEMKE HEINDRYCKX ◽  
YVES-PAUL VANDEWYNCKEL ◽  
LEO A. VAN GRUNSVEN ◽  
HANS VAN VLIERBERGHE
Keyword(s):  
Growth Factor ◽  
Progenitor Cells ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Liver Tumours ◽  
Primary Liver Tumours
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