CX3CR1 promotes recruitment of human glioma-infiltrating microglia/macrophages (GIMs)

Held‐Feindt, Janka; Hattermann, Kirsten; Müerköster, Susanne Sebens; Wedderkopp, Hanna; Knerlich-Lukoschus, Friederike; Ungefroren, Hendrik; Mehdorn, H. Maximilian; Mentlein, Rolf

doi:10.1016/j.yexcr.2010.02.018

Cited by 135 publications

(110 citation statements)

References 55 publications

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“…Genomic DNA was digested by RNase-free DNase (1 U/µl, Promega, Madison, WI, USA), and cDNA was synthesized using RevertAid™ H Minus M-MuLV Reverse Transcriptase (200 U/µl, Fermentas, Vilnius, Lithuania). Real-time RT-PCR was performed as previously described (20) using TaqMan primer probes (Applied Biosystems, Foster City, CA, USA): rGAPDH (Rn99999916_s1), rCXCL12 (Rn00573260_m1), rCXCR4 (Rn00573522_s1), rCXCR7 (Rn00584358_m1), rGFAP (Rn00566603_m1), rSox2 (Rn01286286_g1), rMusashi1 (Rn00596059_m1), rCD133 (Rn00572720_m1), rNestin (Rn00564394_m1). Samples were analyzed in duplicates.…”

Section: Quantitative Rt-pcr (Qrt-pcr)mentioning

confidence: 99%

CXCL12 mediates apoptosis resistance in rat C6 glioma cells

2012

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Abstract. The chemokine CXCL12/stromal cell-derived factor-1 (SDF-1) and its receptor CXCR4 regulate migration and patterning processes during brain development, but also contribute to proliferation and expansion of gliomas, the most malignant brain tumors. Recently, a previous orphan-receptor CXCR7/RDC-1 was discovered to be a second receptor for CXCL12. CXCR7 has been detected in normal brain parenchyma, but in particular in human brain tumors. However, little is known about the functional relevance of CXCR7. Since the well-characterized rat C6 glioma cell line is commonly used as a glioma model in vitro and in vivo, we investigated the expression, regulation and function of CXCL12 and its receptors in these tumor cells. Whereas CXCL12 and CXCR7 were transcribed at notable levels, CXCR4 was quite low. By sublethal doses of temozolomide, an alkylating drug commonly used in adjuvant glioma therapy, transcription of CXCL12 and its receptors were significantly induced. Decreased proliferation resulting from this sublethal treatment with temozolomide could be completely restored to normal proliferation rates by simultaneous stimulation with CXCL12. Similarly, CXCL12 protected C6 cells from apoptosis under treatment with higher temozolomide doses. Thus, the CXCL12-CXCR7 axis promotes glioma progression, and the rat C6 glioma cell line may be a useful model to further investigate these mechanisms in vitro and in vivo.

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Section: Quantitative Rt-pcr (Qrt-pcr)mentioning

confidence: 99%

CXCL12 mediates apoptosis resistance in rat C6 glioma cells

2012

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“…A dynamic relationship forms between the pre-neoplastic/ neoplastic and non-neoplastic stromal cell populations through stromagen and gliomagens release, which together facilitate tumorigenesis, tumor maintenance and glioma progression. endothelial growth factor (Forstreuter et al, 2002;Kerber et al, 2008), hepatocyte growth factor (Badie et al, 1999;Kunkel et al, 2001), monocyte chemoattractant protein-1 (Martinet et al, 1992;Leung et al, 1997) and the chemokine CX3CL1 (fractalkine) through activation of the CX3CR1 receptor (Held-Feindt et al, 2010). Monocyte chemoattractant protein-1 can also increase the surface expression of CX3CR1 on microglia (Green et al, 2006), thus providing amplification circuits for further microglia recruitment.…”

Section: Stromal Determinants Of Glioma Formation and Growthmentioning

confidence: 99%

The ecology of brain tumors: lessons learned from neurofibromatosis-1

Pong

Gutmann

2010

Oncogene

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Traditionally, cancer studies have primarily focused on mutations that activate growth or survival pathways in susceptible pre-neoplastic/neoplastic cells. However, recent research has revealed a critical role for nonneoplastic cells within the tumor microenvironment in the process of cancer formation and progression. In addition, the existence of regional and developmental variations in susceptible cell types and supportive microenvironments support a model of tumorigenesis in which the dynamic symbiotic relationship between neoplastic and non-neoplastic cell types dictate where and when cancers form and grow. In this review, we highlight advances in neurofibromatosis type 1 (NF1) genetically engineered mouse brain tumor (glioma) modeling to reveal how cellular and molecular heterogeneity in both the pre-neoplastic/ neoplastic and non-neoplastic cellular compartments contribute to gliomagenesis and glioma growth.

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“…CX3CL1 is localized in the outer layer of cells of glioblastoma tumorspheres, suggesting the involvement of the chemokine system in intracellular adhesion (Erreni et al, 2010). The high levels of CX3CL1/CX3CR1 results in the recruitment of glioma-infiltrating microglia, which displays high levels of adhesion and migration in vitro; this suggests an important role for the chemokine system in tumor promotion (Held-Feindt et al, 2010).…”

Section: Chemokine (C-x3-c Motif) Ligandmentioning

confidence: 99%