EGFR Cooperates with EGFRvIII to Recruit Macrophages in Glioblastoma

An, Zhenyi; Knobbe-Thomsen, Christiane B.; Wan, Xiaohua; Fan, Qi; Reifenberger, Guido; Weiss, William A.

doi:10.1158/0008-5472.can-17-3551

Cited by 53 publications

(34 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous study has shown that macrophage recruitment plays a key role in GABRP-mediated tumor progression in pancreatic cancer [45]. TAMs also involved in tumor growth in glioblastoma [45,46]. The results from this work highlight several novel features of the mechanisms underlying glioblastoma.…”

Section: Discussionsupporting

confidence: 53%

RETRACTED ARTICLE: SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway

Han

Wei

Guo

et al. 2020

J Exp Clin Cancer Res

View full text Add to dashboard Cite

Background Glioblastoma is a common disease of the central nervous system (CNS), with high morbidity and mortality. In the infiltrate in the tumor microenvironment, tumor-associated macrophages (TAMs) are abundant, which are important factors in glioblastoma progression. However, the exact details of TAMs in glioblastoma progression have yet to be determined. Methods The clinical relevance of SET domain bifurcated 1 (SETDB1) was analyzed by immunohistochemistry, real-time PCR and Western blotting of glioblastoma tissues. SETDB1-induced cell proliferation, migration and invasion were investigated by CCK-8 assay, colony formation assay, wound healing and Transwell assay. The relationship between SETDB1 and colony stimulating factor 1 (CSF-1), as well as TAMs recruitment was examined by Western blotting, real-time PCR and syngeneic mouse model. Results Our findings showed that SETDB1 upregulated in glioblastoma and relative to poor progression. Gain and loss of function approaches showed the SETDB1 overexpression promotes cell proliferation, migration and invasion in glioblastoma cells. However, knockdown SETDB1 exerted opposite effects in vitro. Moreover, SETDB1 promotes AKT/mTOR-dependent CSF-1 induction and secretion, which leads to macrophage recruitment in the tumor, resulted in tumor growth. Conclusion Our research clarified that SETDB1 regulates of tumor microenvironment and hence presents a potential therapeutic target for treating glioblastoma.

show abstract

Section: Discussionsupporting

confidence: 53%

RETRACTED ARTICLE: SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway

Han

Wei

Guo

et al. 2020

J Exp Clin Cancer Res

View full text Add to dashboard Cite

show abstract

“…Of note, several items of the list of genes with enhanced expression in Tum HIGH cells encoded proteins previously implicated in GBM cell aggressiveness (e.g. E2F1 [71], EGFR [1], NOTCH1 [7], FABP7 [15], PTPRZ1 [25]). Conversely, genes with known tumor-suppressor properties were identified among the genes overexpressed in Tum LOW cells (e.g.…”

Section: Resultsmentioning

confidence: 99%

Capture at the single cell level of metabolic modules distinguishing aggressive and indolent glioblastoma cells

Saurty-Seerunghen

Bellenger

El-Habr

et al. 2019

acta neuropathol commun

View full text Add to dashboard Cite

Glioblastoma cell ability to adapt their functioning to microenvironment changes is a source of the extensive intra-tumor heterogeneity characteristic of this devastating malignant brain tumor. A systemic view of the metabolic pathways underlying glioblastoma cell functioning states is lacking. We analyzed public single cell RNA-sequencing data from glioblastoma surgical resections, which offer the closest available view of tumor cell heterogeneity as encountered at the time of patients’ diagnosis. Unsupervised analyses revealed that information dispersed throughout the cell transcript repertoires encoded the identity of each tumor and masked information related to cell functioning states. Data reduction based on an experimentally-defined signature of transcription factors overcame this hurdle. It allowed cell grouping according to their tumorigenic potential, regardless of their tumor of origin. The approach relevance was validated using independent datasets of glioblastoma cell and tissue transcriptomes, patient-derived cell lines and orthotopic xenografts. Overexpression of genes coding for amino acid and lipid metabolism enzymes involved in anti-oxidative, energetic and cell membrane processes characterized cells with high tumorigenic potential. Modeling of their expression network highlighted the very long chain polyunsaturated fatty acid synthesis pathway at the core of the network. Expression of its most downstream enzymatic component, ELOVL2, was associated with worsened patient survival, and required for cell tumorigenic properties in vivo. Our results demonstrate the power of signature-driven analyses of single cell transcriptomes to obtain an integrated view of metabolic pathways at play within the heterogeneous cell landscape of patient tumors.

show abstract

“…120 Similarly, Andre-Gregoire et al 121 observed a higher concentration of EVs in patients with GBM, as well as showing that EVs from patientderived glioblastoma stem cells, which are thought to be involved in tumour initiation, expansion, resistance to treatments and relapse, had increased cargo relating to cell adhesion after TMZ treatment, indicating that TMZ had the potential to promote the increased release of factors favouring tumour progression. 121 Manda et al 124 123 Also, the presence of EGFRvIII in exosomes correlated with a lower overall survivor pattern-21.1 months-compared with 28.6 months for patients with no EGFRvIII expression in exosomes. 124 Chandran et al 125 reported that syndecan-1 found in plasma EVs can be used to distinguish low-grade glioma from high-grade GBM with a sensitivity of 71% and a specificity of 80%, and provided strong support for plasma-EV-derived syndecan-1 being derived from GBM tumours.…”

Section: Microvesicles In Glioblastomamentioning

confidence: 96%

Circulating biomarkers in patients with glioblastoma

et al. 2019

View full text Add to dashboard Cite

Gliomas are the most common tumours of the central nervous system and the most aggressive form is glioblastoma (GBM). Despite advances in treatment, patient survival remains low. GBM diagnosis typically relies on imaging techniques and postoperative pathological diagnosis; however, both procedures have their inherent limitations. Imaging modalities cannot differentiate tumour progression from treatment-related changes that mimic progression, known as pseudoprogression, which might lead to misinterpretation of therapy response and delay clinical interventions. In addition to imaging limitations, tissue biopsies are invasive and most of the time cannot be performed over the course of treatment to evaluate 'real-time' tumour dynamics. In an attempt to address these limitations, liquid biopsies have been proposed in the field. Blood sampling is a minimally invasive procedure for a patient to endure and could provide tumoural information to guide therapy. Tumours shed tumoural content, such as circulating tumour cells, cell-free nucleic acids, proteins and extracellular vesicles, into the circulation, and these biomarkers are reported to cross the blood-brain barrier. The use of liquid biopsies is emerging in the field of GBM. In this review, we aim to summarise the current literature on circulating biomarkers, namely circulating tumour cells, circulating tumour DNA and extracellular vesicles as potential non-invasively sampled biomarkers to manage the treatment of patients with GBM.

show abstract

EGFR Cooperates with EGFRvIII to Recruit Macrophages in Glioblastoma

Cited by 53 publications

References 31 publications

RETRACTED ARTICLE: SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway

RETRACTED ARTICLE: SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway

Capture at the single cell level of metabolic modules distinguishing aggressive and indolent glioblastoma cells

Circulating biomarkers in patients with glioblastoma

Contact Info

Product

Resources

About