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 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 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 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.

scholarly journals Knockdown of USF1 Inhibits the Vasculogenic Mimicry of Glioma Cells via Stimulating SNHG16/miR-212-3p and linc00667/miR-429 Axis

2019 ◽  
Vol 14 ◽  
pp. 465-482 ◽  
Author(s):  
Di Wang ◽  
Jian Zheng ◽  
Xiaobai Liu ◽  
Yixue Xue ◽  
Libo Liu ◽  
...  
Keyword(s):  
Vasculogenic Mimicry ◽  
Glioma Cells

scholarly journals The embryonic stem cell microenvironment inhibits mouse glioma cell proliferation by regulating PI3K/AKT pathway

2020 ◽  
Author(s):  
xiongjun He ◽  
jiahui liu ◽  
xiaoran wang ◽  
tengfei liu ◽  
liu yang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Embryonic Stem Cell ◽  
Signaling Pathway ◽  
Vasculogenic Mimicry ◽  
Embryonic Stem ◽  
Glioma Cells ◽  
Control Group ◽  
Regulatory Factors ◽  
Mouse Glioma

Abstract PURPOSETo study the effect of the embryonic stem cell (ESc) microenvironment in inhibiting mouse glioma cells and its possible mechanism. METHODSGlioblastoma cell line U118 in the brain, was investigated in this study. There were four experimental groups: U118 glioma cells cultured alone as the control group (GB group), U118 cell and ESc co-cultured group(GE group), U118 cell and ESc co-cultured and adding phosphoinositide 3-kinase (PI3K) agonist group (GA group), U118 and temozolomide as the positive control group (GT group); U118 cells were harvested after 72 hours of culture. Cell proliferation, apoptosis, reactive oxygen species (ROS) and vasculogenic mimicry assays, quantitative real-time RT-PCR (qPCR), and western blot (WB) were study, the biological function of U118 glioma cells and the PI3K/AKT signaling pathway were compared the differences between the groups. RESULTSCompared with the GB control group, the GE co-culture group and GT chemotherapy group showed reduced cell proliferation, increased apoptosis, increased ROS, decreased or disappearance of vasculogenic mimicry. Expression of cyclin B and D, significantly reduced, while that of BAX, BCL-2, P53, Caspase3, Gsk-3B, P21, and P27, significantly increased. The expression of PI3K, PDK, AKT, and mTOR, significantly decreased while that of PTEN significantly increased. The expression of positive regulatory factors significantly increased but negative regulatory factors decreased in GA group compared to the GE group. CONCLUSIONThe ESC microenvironment reverse glioma malignancy, partially via inhibition of the PI3K signaling pathway. Our study may have a significant impact and clinical implication on cell therapy in glioma.

scholarly journals SUMOylation of IGF2BP2 Promotes Vasculogenic Mimicry of Glioma Via Regulating OIP5-AS1/miR-495-3p

2021 ◽  
Author(s):  
Hao Li ◽  
Di Wang ◽  
Bolong Yi ◽  
Heng Cai ◽  
Yipeng Wang ◽  
...  
Keyword(s):  
Western Blot ◽  
Nude Mice ◽  
Vasculogenic Mimicry ◽  
Three Dimensional ◽  
Glioma Cells ◽  
Luciferase Reporter ◽  
Post Translational Modification ◽  
Culture Methods ◽  
Angiogenic Therapy

Abstract Background: Glioma is the most common primary malignant tumor of human central nervous system, and its rich vascular characteristics make anti-angiogenic therapy become a therapeutic hotspot. However, the existence of glioma VM makes the anti-angiogenic therapy ineffective. SUMOylation is a post-translational modification that affects cell tumorigenicity by regulating the expression and activity of substrate proteins.Methods: The binding and modification of IGF2BP2 and SUMO1were identified using Ni2+-NTA agarose bead pull-down assays, CO-IP and western blot; and in vitro SUMOylation assays combined with immunoprecipitation and Immunofluorescence staining were performed to explore the detail affects and regulations of the SUMOylation on IGF2BP2. RT-PCR and western blot were used to detect the expression levels of IGF2BP2, OIP5-AS1, and miR-495-3p in glioma tissues and cell lines. CCK-8 assays, cell transwell assays, and three-dimensional cell culture methods were used for evaluating the function of IGF2BP2, OIP5-AS1, miR-495-3p, HIF1A and MMP14 in biological behaviors of glioma cells. Meantime, RIP and luciferase reporter assays were used forinquiring into the interactions among IGF2BP2, OIP5-AS1, miR-495-3p, HIF1A and MMP14. Eventually, the tumor xenografts in nude mice further ascertained the effects of IGF2BP2 SUMOylation on glioma cells.Results: This study proved that IGF2BP2 mainly binds to SUMO1 and was SUMOylated at the lysine residues K497, K505 and K509 sites, which can be reduced by SENP1. SUMOylation increased IGF2BP2 protein expression and blocked its degradation through ubiquitin-proteasome pathway, thereby increasing its stability. The expressions of IGF2BP2 and OIP5-AS1 were up-regulated and the expression of miR-495-3p was down-regulated in both glioma tissues and cells. IGF2BP2 enhances the stability of OIP5-AS1, thereby increasing the binding of OIP5-AS1 to miR-495-3p, weakening the binding of miR-495-3p to the 3’UTR of HIF1A and MMP14 mRNA, and ultimately promoting the formation of VM in glioma.Conclusions: This study first revealed that SUMOylation of IGF2BP2 regulated OIP5-AS1/miR-495-3p to promote VM formation in glioma cells and xenografts growth in nude mice, providing a new idea for molecular targeted therapy of glioma.

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