scholarly journals M2-like tumor-associated macrophages drive vasculogenic mimicry through amplification of IL-6 expression in glioma cells

Oncotarget ◽  
2016 ◽  
Vol 8 (1) ◽  
pp. 819-832 ◽  
Author(s):  
Lin Zhang ◽  
Yangyang Xu ◽  
Jintang Sun ◽  
Weiliang Chen ◽  
Lei Zhao ◽  
...  
Keyword(s):  
Vasculogenic Mimicry ◽  
Glioma Cells ◽  
Tumor Associated Macrophages

scholarly journals SUMOylation of PUM2 promotes the vasculogenic mimicry of glioma cells via regulating CEBPD

2020 ◽  
Vol 10 (5) ◽  
Author(s):  
Di Wang ◽  
Xuelei Ruan ◽  
Xiaobai Liu ◽  
Yixue Xue ◽  
Lianqi Shao ◽  
...  
Keyword(s):  
Vasculogenic Mimicry ◽  
Glioma Cells

scholarly journals Tumor associated macrophages and its nanovesicles: Immunological insights in cerebral glioma

2020 ◽  
Vol 10 (1) ◽  
pp. 14
Author(s):  
Turano E ◽  
Farinazzo A ◽  
El Mously S ◽  
Calabria F ◽  
Jugerson I ◽  
...  
Keyword(s):  
Glioma Cells ◽  
Annexin V ◽  
Low Grade ◽  
Cerebral Glioma ◽  
Tumor Associated Macrophages ◽  
Cellular Activation ◽  
Protein Assay ◽  
Glioma Progression

Purpose: The immune system has a key role in glioma progression, especially the tumor associated macrophages (TAMs). In-vivo, we aimed to study the total TAMs and differential M1 and M2 TAM infiltration in low grade (LGG) versus high grade gliomas (HGG). Also, we investigated the implication of total TAMs and differential M1 and M2 TAMs infiltration on glioma progression. In-vitro, we studied the effect of soluble factors present in nanovesicles (NV) released from M1 TAMs on the fate of glioma cells.Methods: In-vivo, we performed immunohistochemistry using iNOS and CD163 (markers for M1 and M2 respectively). In-vitro, we polarized the human monocytes U937 cell line into M1, we isolated the NV from the M1-conditioned medium (CM) by centrifugation and filtration; then, the protein content of the NV was quantified by the protein assay. We added M1-NV on U251 glioma cells and we studied the cellular activation of glioma cells using the MTT assay. To assess the apoptosis of U251, we used the flow-cytometry. Apoptotic cells were identified by annexin V and Propidium Iodide (markers for early and late apoptosis respectively).Results: in-vivo, there is an M1/M2 imbalance in early stages of glioma which is associated with earlier progression to high malignancy. Also, the higher M2 infiltration, the earlier is the progression. In-vitro, M1-NV had a more potent anti-tumor effect compared to its corresponding CM. We assume that our experimental results can be a future treatment for the cerebral glioma.

scholarly journals MicroRNA-Let-7f reduces the vasculogenic mimicry of human glioma cells by regulating periostin-dependent migration

2016 ◽  
Vol 35 (3) ◽  
pp. 1771-1777 ◽  
Author(s):  
HAO XUE ◽  
XIAO GAO ◽  
SHUGANG XU ◽  
JINSEN ZHANG ◽  
XING GUO ◽  
...  
Keyword(s):  
Vasculogenic Mimicry ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells

scholarly journals HNRNPD interacts with ZHX2 regulating the vasculogenic mimicry formation of glioma cells via linc00707/miR-651-3p/SP2 axis

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Sifei Yu ◽  
Xuelei Ruan ◽  
Xiaobai Liu ◽  
Fangfang Zhang ◽  
Di Wang ◽  
...  
Keyword(s):  
Rna Binding ◽  
Rna Binding Proteins ◽  
Vasculogenic Mimicry ◽  
Glioma Cells ◽  
Specific Protein ◽  
The Cancer Genome Atlas ◽  
Migration And Invasion ◽  
Promoter Regions ◽  
The Stability ◽  
Nuclear Ribonucleoprotein

AbstractStudies have found that RNA-binding proteins (RBPs) are dysfunctional and play a significant regulatory role in the development of glioma. Based on The Cancer Genome Atlas database and the previous studies, we selected heterogeneous nuclear ribonucleoprotein (HNRNPD) as the research candidate and sought its downstream targeted genes. In the present study, HNRNPD, linc00707, and specific protein 2 (SP2) were highly expressed, while zinc fingers and homeboxes 2 (ZHX2) and miR-651-3p were remarkedly downregulated in glioma tissues and cells. HNRNPD, linc00707, and SP2 knockdown or ZHX2 and miR-651-3p overexpression suppressed glioma cells proliferation, migration, and invasion and vasculogenic mimicry (VM) formation. Knockdown of HNRNPD increased the stability of ZHX2 mRNA. ZHX2 bound to the promoter region of linc00707 and negatively regulate its expression. Linc00707 could bind with miR-651-3p, while miR-651-3p bound to the 3′ untranslated region (3′UTR) of SP2 mRNA to negatively regulate its expression. The transcription factor SP2 directly bound to the promoter regions of the VM formation-related proteins MMP2, MMP9, and VE-cadherin, playing a role in promoting transcription in order to regulate the VM formation ability of glioma cells.

scholarly journals Plasminogen Kringle 5–Engineered Glioma Cells Block Migration of Tumor-Associated Macrophages and Suppress Tumor Vascularization and Progression

2005 ◽  
Vol 65 (18) ◽  
pp. 8359-8365 ◽  
Author(s):  
Sabrina R. Perri ◽  
Josephine Nalbantoglu ◽  
Borhane Annabi ◽  
Zafiro Koty ◽  
Laurence Lejeune ◽  
...  
Keyword(s):  
Glioma Cells ◽  
Tumor Vascularization ◽  
Tumor Associated Macrophages ◽  
Kringle 5

scholarly journals Biosynthetic circ-PLEKHA5 stabilized by SRSF7 promotes the vasculogenic mimicry of glioblastoma cells by encoding a novel protein 622aa

2020 ◽  
Author(s):  
Rui Su ◽  
Xiaobai Liu ◽  
Hao Teng ◽  
Xuelei Ruan ◽  
Di Wang ◽  
...  
Keyword(s):  
Vasculogenic Mimicry ◽  
Glioma Cells ◽  
Immunofluorescence Assay ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Glioblastoma Cells ◽  
Associated Proteins ◽  
Novel Strategy ◽  
Novel Protein

Abstract Background: Increasing studies have been demonstrated that circRNAs play vital regulatory roles in the biological behaviors of glioblastoma cells, and increasing circRNAs are found to have the capacity of encoding small peptides, which are involved in the regulatory process.Methods: Western blot and qRT-PCR were conducted to confirm the expression of SRSF7 and circ-PLEKHA5 respectively. RNase R digestion assay and fluorescence in situ hybridization assays were conducted to evaluate the existence and cellular location of circ-PLEKHA5. RIP assay was used to access the relationship between SRSF7 and circ-PLEKHA5. Dual-luciferase assay and FLAG tag assays were performed to test the coding capability of circ-PLEKHA5. Immunofluorescence assay was conducted to evaluate the location of circ-PLEKHA5-622aa. CCK-8, vasculogenic mimicry (VM) formation and transwell assays were used to evaluate the roles of SRSF7, circ-PLEKHA5, circ-PLEKHA5-622aa on proliferation, VM formation, migration and invasion. Nude mice xenograft studys with PAS-CD34 staining were used to clarify the functional roles of SRSF7 and circ-PLEKHA5 on VM formation in vivo.Results: SRSF7 was up-regulated in glioma, and promoted the proliferation, migration, invasion, VM formation and the expression of VM-associated proteins of glioma cells by increasing the expression of circ-PLEKHA5. Circ-PLEKHA5 was mainly localized in cytoplasm and promoted the proliferation, migration, invasion, VM formation and the expression of VM-associated proteins of glioma cells by encoding a novel protein circ-PLEKHA5-622aa. The application of SRSF7 and circ-PLEKHA5 inhibitor significantly suppressed the tumor growth and VM formation in vivo.Conclusions: This study first demonstrated the coding ability of circ-PLEKHA5, and identified the regulatory roles of SRSF7/circ-PLEKHA5/circ-PLEKHA5-622aa pathway in VM formation of glioblastoma cells. Our findings might provide a novel strategy for glioma treatment.

scholarly journals Tenascin-c mediated vasculogenic mimicry formation via regulation of MMP2/MMP9 in glioma

2019 ◽  
Vol 10 (12) ◽  
Author(s):  
Hai-ping Cai ◽  
Jing Wang ◽  
Shao-yan Xi ◽  
Xiang-rong Ni ◽  
Yin-sheng Chen ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Vasculogenic Mimicry ◽  
Glioma Cells ◽  
Matrix Metalloproteinase 2 ◽  
Potential Therapeutic Target ◽  
Akt Phosphorylation ◽  
Tenascin C ◽  
And Migration

AbstractVasculogenic mimicry (VM), the formation of vessel-like structures by highly invasive tumor cells, has been considered one of several mechanisms responsible for the failure of anti-angiogenesis therapy in glioma patients. Therefore, inhibiting VM formation might be an effective therapeutic method to antagonize the angiogenesis resistance. This study aimed to show that an extracellular protein called Tenascin-c (TNC) is involved in VM formation and that TNC knockdown inhibits VM in glioma. TNC was upregulated with an increase in glioma grade. TNC and VM formation are potential independent predictors of survival of glioma patients. TNC upregulation was correlated with VM formation, and exogenous TNC stimulated VM formation. Furthermore, TNC knockdown significantly suppressed VM formation and proliferation in glioma cells in vitro and in vivo, with a reduction in cellular invasiveness and migration. Mechanistically, TNC knockdown decreased Akt phosphorylation at Ser473 and Thr308 and subsequently downregulated matrix metalloproteinase 2 and 9, both of which are important proteins associated with VM formation and migration. Our results indicate that TNC plays an important role in VM formation in glioma, suggesting that TNC is a potential therapeutic target for anti-angiogenesis therapy for glioma.

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