Survival and invasiveness of astrocytomas promoted by erythropoietin

Mohyeldin, Ahmed; Dalgard, Clifton L.; Lu, Hongyang; McFate, Thomas; Tait, Angela; Patel, Viral C.; Wong, Karen; Rushing, E J; Roy, Subhojit; Ács, Géza; Verma, Ajay

doi:10.3171/jns.2007.106.2.338

Cited by 33 publications

(30 citation statements)

References 65 publications

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“…Similarly, EPO did not promote tumor growth in nude mice after subcutaneous transplantation of another glioma cell line, HTZ11 (22). In some contrast with the present findings, EPO was reported to promote invasiveness of glioma cells under basal conditions (27). This discrepant result may be explained by the use of a different glioma cell line (U251) and a different assay system (matrigel invasion chamber), but most importantly of a high dose of EPO (27), which cannot be expected to be reached in the brain on peripheral application.…”

Section: Discussioncontrasting

confidence: 85%

“…In some contrast with the present findings, EPO was reported to promote invasiveness of glioma cells under basal conditions (27). This discrepant result may be explained by the use of a different glioma cell line (U251) and a different assay system (matrigel invasion chamber), but most importantly of a high dose of EPO (27), which cannot be expected to be reached in the brain on peripheral application. In fact, the concentrations used in the present study were chosen according to data on penetration of EPO over the blood-brain barrier (7,41).…”

Section: Discussioncontrasting

confidence: 78%

“…EPO was reported to promote growth of different tumor cell lines as well as primary human tumor cells (23)(24)(25)(26). Data on glioma cell lines and EPO are scarce (27)(28)(29), reporting that EPO protects cultured glioma cell lines from radiation-or cisplatin-induced cytotoxicity (24,27) or from starvation-provoked (serum deprivation) cell death via activation of antiapoptotic pathways (29).…”

Section: Introductionmentioning

confidence: 98%

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Erythropoietin Augments Survival of Glioma Cells After Radiation and Temozolomide

Hassouna

Sperling

Kim

et al. 2008

International Journal of Radiation Oncology*Biology*Physics

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Section: Discussioncontrasting

confidence: 85%

Section: Discussioncontrasting

confidence: 78%

Section: Introductionmentioning

confidence: 98%

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Erythropoietin Augments Survival of Glioma Cells After Radiation and Temozolomide

Hassouna

Sperling

Kim

et al. 2008

International Journal of Radiation Oncology*Biology*Physics

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“…However, further studies are needed with more specific antibodies and greater sample numbers to determine the prognostic significance of EpoR expression on tumors. The biological effects of Epo stimulation of tumor cells is still debated with reports of enhanced survival (8,11), proliferation (4,6,(38)(39)(40), resistance to treatment (38,41,42), tumor angiogenesis (43)(44)(45), chemotaxis (46), invasion (47)(48)(49)(50), and migration (40,46,51). Others have reported no discernible effects of Epo (52).…”

Section: Discussionmentioning

confidence: 99%

Erythropoietin-Induced Activation of the JAK2/STAT5, PI3K/Akt, and Ras/ERK Pathways Promotes Malignant Cell Behavior in a Modified Breast Cancer Cell Line

Shi

Hodges

Dunlop

et al. 2010

Molecular Cancer Research

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Erythropoietin (Epo), the major regulator of erythropoiesis, and its cognate receptor (EpoR) are also expressed in nonerythroid tissues, including tumors. Clinical studies have highlighted the potential adverse effects of erythropoiesis-stimulating agents when used to treat cancer-related anemia. We assessed the ability of EpoR to enhance tumor growth and invasiveness following Epo stimulation. A benign noninvasive rat mammary cell line, Rama 37, was used as a model system. Cell signaling and malignant cell behavior were compared between parental Rama 37 cells, which express few or no endogenous EpoRs, and a modified cell line stably transfected with human EpoR (Rama 37-28). The incubation of Rama 37-28 cells with pharmacologic levels of Epo led to the rapid and sustained increases in phosphorylation of signal transducers and activators of transcription 5, Akt, and extracellular signal-regulated kinase. The activation of these signaling pathways significantly increased invasion, migration, adhesion, and colony formation. The Epo-induced invasion capacity of Rama 37-28 cells was reduced by the small interfering RNA-mediated knockdown of EpoR mRNA levels and by inhibitors of the phosphoinositide 3-kinase/Akt and Ras/extracellular signal-regulated kinase signaling pathways with adhesion also reduced by Janus-activated kinase 2/signal transducers and activators of transcription 5 inhibition. These data show that Epo induces phenotypic changes in the behavior of breast cancer cell lines and establishes links between individual cell signaling pathways and the potential for cancer spread. Mol Cancer Res; 8(4); 615-26. ©2010 AACR.

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“…The cytotoxic effect of these two agents is reduced by EPO in vitro [39] . EPO also promotes the growth and the survival of astrocytoma cells in vitro, as it acts against the cytotoxic effect of chemical agents, such as cisplatin [40] . EPO acts cytoprotectively and prevents apoptosis of ischemic heart through activation of the JAK/STAT and RAS/MAPK pathways through cardiac AKT activity [41] .…”

Section: Discussionmentioning

confidence: 99%

In vitro and in vivo Cytogenetic Effects of Recombinant Human Erythropoietin on the Frequency of Sister Chromatid Exchanges Alone or in Combination with Mitomycin C

Digkas

Chrisafi²,

Passadaki³

et al. 2010

Chemotherapy

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Background: Erythropoietin (EPO) is a glycoprotein which has a main property, erythropoiesis, but its range of action in the human body is very wide. It has been suggested that EPO acts cytoprotectively for many cell lines against many toxic causes in vitro and in vivo. Our aim was to study the action of EPO on DNA of two cell types, human lymphocytes in vitro and on P388 ascites tumor cells inoculated in BDF1 mice in the presence and absence of the genotoxic agent mitomycin C (MMC). Method: The sister chromatid exchange (SCE) assay was used as it is a very sensitive, simple and rapid method for detecting DNA damage. Proliferation rate indices (PRI) and mitotic indices (MI) were also counted. Results: EPO did not alter the SCE level when it acted alone on both cell lines. MMC as a potent genotoxic agent increased SCE levels in vitro and in vivo. EPO used in combination with MMC significantly decreased SCE levels and increased PRI and MI values induced by MMC alone both in vitro and in vivo. Conclusions: EPO acts protectively against the genotoxic potential of MMC, and this action may have clinical implications.

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Survival and invasiveness of astrocytomas promoted by erythropoietin

Abstract: Hypoxia-inducible autocrine and paracrine EPO signaling participates in the malignant progression of GBMs.

Cited by 33 publications

References 65 publications

Erythropoietin Augments Survival of Glioma Cells After Radiation and Temozolomide

Erythropoietin Augments Survival of Glioma Cells After Radiation and Temozolomide

Erythropoietin-Induced Activation of the JAK2/STAT5, PI3K/Akt, and Ras/ERK Pathways Promotes Malignant Cell Behavior in a Modified Breast Cancer Cell Line

In vitro and in vivo Cytogenetic Effects of Recombinant Human Erythropoietin on the Frequency of Sister Chromatid Exchanges Alone or in Combination with Mitomycin C

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