Expression of functional granulocyte colony-stimulating factor receptors on human B-lymphocytic leukemia cells

Abstract

We analyzed the expression of cell surface antigens and granulocyte colony-stimulating factor (G-CSF) receptors using flow cytometry, the expression of G-CSF mRNA receptor, using reverse transcription (RT)-PCR, and tested the effect of G-CSF on leukemia colony formation. A total of 14 lymphocytic leukemia patients were examined, seven with acute lymphocytic leukemia (ALL), two with adult T-cell leukemia (ATL), two with B-chronic lymphocytic leukemia (CLL), two with chronic myelocytic leukemia in lymphoid blastic crisis (CML-LBC), and one with plasma cell leukemia (PCL). The presence of G-CSF receptors was demonstrated in 4/14 (29%) patients, two with ALL, one with CLL, and one with CML-LBC, and was associated with stimulation of leukemia clonogenic cell growth by G-CSF. In addition, all four positive leukemia cell types expressed typical B-cell antigens. Our results indicated that G-CSF receptors are expressed on some portion of B-lymphoid leukemia and that their receptors are functional as growth stimulators.

Pro-inflammatory-Related Loss of CXCL12 Niche Promotes Acute Lymphoblastic Leukemic Progression at the Expense of Normal Lymphopoiesis

“…Remarkably, the cellular communication between leukemic cells and MSC through exosomes or across nanotubes (65, 66) and the disruption of the CXCR4/CXCL12 axis (28, 59), suggesting a key role for G-CSF in this phenomena, are consistent with our previous reports about production of pro-inflammatory factors by tumor cells (30), related to G-CSF and Gfi-1 (29). Accordingly, G-CSF administration in a preclinical model of ALL showed an increased tumor burden (67), and its mechanism may be operating in the niche because B cell malignances rarely expressed G-CSF receptor and are unable to respond in vitro to this cytokine (68). In contrast, in vitro normal B-cell production in a stromal-free model is more efficient when G-CSF is supplied (69).…”

The granulocyte colony stimulating factor (G‐CSF) activates Jak/STAT and MAPK pathways in a trophoblastic cell line

“…G-CSF exerts its biological activities through its interaction with a specific receptor expressed on the surface of target cells, the G-CSFR, which is a member of the hematopoietic receptor superfamily [Morstyng and Burgess, 1988;Nicola, 1989;Demetri and Griffin, 1991]. The presence of G-CSFR has been reported in normal myeloid progenitors, mature neutrophils and some myeloid and lymphocytic leukemia cell lines [Nicola and Metcalf, 1985;Begley et al, 1988;Shimoda et al, 1992;Shinjo et al, 1995;Handa et al, 2000]. In addition, G-CSFR has also been detected in non-hematopoietic tissues, including endothelial cells [Bussolino et al, 1989], cardiomyocytes and cardiac fibroblasts [Harada et al, 2005], neural stem cells [Jung et al, 2006], trophoblastic cells and human placenta [Uzumaki et al, 1989;Shorter et al, 1992;Mc Cracken et al, 1996].…”

Expression and role of granulocyte macrophage colony-stimulating factor receptor (GM-CSFR) and granulocyte colony-stimulating factor receptor (G-CSFR) on Ph-positive acute B lymphoblastic leukemia

“…In previous studies, researchers have demonstrated that certain subgroups of B-lymphocytic leukemia cells express functional G-CSFR or GM-CSFR [10][11][12][13]. It deserves to be mentioned that Ph-positive acute lymphoblastic leukemia (ph + ALL) presents a distinctive expression pattern of G-CSGR and GM-CSFR and responds to the stimulation of G-CSF and GM-CSF [14][15][16][17][18].…”