Vasculogenic mimicry formation in EBV-associated epithelial malignancies

Xiang, Tong; Lin, Yu Xin; Ma, Wenlong; Zhang, Hao Jiong; Chen, Ke Ming; He, Gui; Zhang, Xiao; Xu, Miao; Feng, Qi Sheng; Chen, Ming Yuan; Zeng, Mu Sheng; Zeng, Yi Xin; Feng, Lin

doi:10.1038/s41467-018-07308-5

Cited by 143 publications

(130 citation statements)

References 60 publications

(88 reference statements)

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“…Thus tumor cells and tissues obtain blood supply [2,40]. The criteria of the VM structure are as follows: (1) absence of vascular endothelial cells on the inner wall of the VM blood vessel; (2) vascular-like channels are lined with tumor cells; (3) positive for PAS staining but negative for CD31 staining, while the endothelial vascular channels are negative for PAS staining but positive for CD31 staining; (4) erythrocytes in the vascular-like channels [44,45]. Patient-derived xenografts models have been used to dissect the mechanisms responsible for VM and tumor progression.…”

Section: Different Forms Of Tumor Angiogenesismentioning

confidence: 99%

Vasculogenic mimicry in carcinogenesis and clinical applications

et al. 2020

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Distinct from classical tumor angiogenesis, vasculogenic mimicry (VM) provides a blood supply for tumor cells independent of endothelial cells. VM has two distinct types, namely tubular type and patterned matrix type. VM is associated with high tumor grade, tumor progression, invasion, metastasis, and poor prognosis in patients with malignant tumors. Herein, we discuss the recent studies on the role of VM in tumor progression and the diverse mechanisms and signaling pathways that regulate VM in tumors. Furthermore, we also summarize the latest findings of non-coding RNAs, such as lncRNAs and miRNAs in VM formation. In addition, we review application of molecular imaging technologies in detection of VM in malignant tumors. Increasing evidence suggests that VM is significantly associated with poor overall survival in patients with malignant tumors and could be a potential therapeutic target.

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Section: Different Forms Of Tumor Angiogenesismentioning

confidence: 99%

Vasculogenic mimicry in carcinogenesis and clinical applications

et al. 2020

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“…And phosphorylation of forkhead box protein O1 (FoxO1), which is transferred from the nucleus to the cytoplasm, prevents FoxO1 from acting on HIF-α (Fig. 1 b) [ 19 , 69 ]. Recent studies have shown that up-regulated expression of interleukin-1β (IL-1β) secreted by B cells promotes the activation of HIF-2α, and HIF-2α activation further promotes the activation of delta like canonical Notch ligand 4 (DLL4) signaling, and finally interact with neurogenic locus notch homolog (Notch) to form the IL-1β/HIF-2α/Notch 1 axis [ 70 ].…”

Section: Canonical and Non-canonical Regulation Of Hif Signalingmentioning

confidence: 99%

Epigenetic crosstalk between hypoxia and tumor driven by HIF regulation

Mao

Wang

et al. 2020

J Exp Clin Cancer Res

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Hypoxia is the major influence factor in physiological and pathological courses which are mainly mediated by hypoxia-inducible factors (HIFs) in response to low oxygen tensions within solid tumors. Under normoxia, HIF signaling pathway is inhibited due to HIF-α subunits degradation. However, in hypoxic conditions, HIF-α is activated and stabilized, and HIF target genes are successively activated, resulting in a series of tumour-specific activities. The activation of HIFs, including HIF-1α, HIF-2α and HIF-3α, subsequently induce downstream target genes which leads to series of responses, the resulting abnormal processes or metabolites in turn affect HIFs stability. Given its functions in tumors progression, HIFs have been regarded as therapeutic targets for improved treatment efficacy. Epigenetics refers to alterations in gene expression that are stable between cell divisions, and sometimes between generations, but do not involve changes in the underlying DNA sequence of the organism. And with the development of research, epigenetic regulation has been found to play an important role in the development of tumors, which providing accumulating basic or clinical evidences for tumor treatments. Here, given how little has been reported about the overall association between hypoxic tumors and epigenetics, we made a more systematic review from epigenetic perspective in hope of helping others better understand hypoxia or HIF pathway, and providing more established and potential therapeutic strategies in tumors to facilitate epigenetic studies of tumors.

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“…They also employed whole-genome, transcriptome, and epigenome sequence analyses of EBVinfected or noninfected AGS cells together with primary samples to comprehensively reveal that EBV infection alters host gene expression through methylation and affects five prominent networks [153]. Apart from the methylation of host cells, EBV could promote vasculogenic mimicry formation, a new tumor vascular paradigm independent of endothelial cells, in NPC and GC cells through the PI3K/ AKT/mTOR/HIF-1α axis [154].…”

Section: Genetic and Epigenetic Abnormalities Of Host Cells In Ebvagcmentioning

confidence: 99%

Gastric cancer: genome damaged by bugs

et al. 2020

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Gastric cancer (GC) is one of the leading causes of cancer-related death worldwide. The role of the microorganisms in gastric tumorigenesis attracts much attention in recent years. These microorganisms include bacteria, virus, and fungi. Among them, Helicobacter pylori (H. pylori) infection is by far the most important risk factor for GC development, with special reference to the early-onset cases. H. pylori targets multiple cellular components by utilizing various virulence factors to modulate the host proliferation, apoptosis, migration, and inflammatory response. Epstein-Barr virus (EBV) serves as another major risk factor in gastric carcinogenesis. The virus protein, EBER noncoding RNA, and EBV miRNAs contribute to the tumorigenesis by modulating host genome methylation and gene expression. In this review, we summarized the related reports about the colonized microorganism in the stomach and discussed their specific roles in gastric tumorigenesis. Meanwhile, we highlighted the therapeutic significance of eradicating the microorganisms in GC treatment.

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Vasculogenic mimicry formation in EBV-associated epithelial malignancies

Cited by 143 publications

References 60 publications

Vasculogenic mimicry in carcinogenesis and clinical applications

Vasculogenic mimicry in carcinogenesis and clinical applications

Epigenetic crosstalk between hypoxia and tumor driven by HIF regulation

Gastric cancer: genome damaged by bugs

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