HIF-1α induces VE-cadherin expression and modulates vasculogenic mimicry in esophageal carcinoma cells

Tang, Nana; Zhu, Hong; Zhang, Hongjie; Zhang, Weifeng; Jin, Huanhuan; Wang, Lu; Wang, Pin; He, Guijun; Bo, Hao; Shi, Ruihua

doi:10.3748/wjg.v20.i47.17894

Cited by 50 publications

(44 citation statements)

References 36 publications

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“…6a,b). Although loss of chromosome 17p (harbouring TP53 , seen in 50–60% of SCLC30) was not seen in this patient, targeted sequencing of their ctDNA identified non-synonymous TP53 and RB1 mutations (Supplementary Table 5) in keeping with the frequent mutation of these genes in SCLC34.…”

Section: Resultsmentioning

confidence: 56%

“…These studies also demonstrated that depletion of VE-cadherin from C8161 cells, led to abrogation of VM network formation in vitro and VM in vivo 20. Subsequent studies validated a functional role of VE-cadherin in glioblastoma and oesophageal cancer VM3435. To address the role of VE-cadherin in SCLC VM, a panel of SCLC cell lines were screened for VE-cadherin expression and NCI-H446 (H446) was selected for functional studies (Fig.…”

Section: Resultsmentioning

confidence: 93%

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Vasculogenic mimicry in small cell lung cancer

et al. 2016

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Small cell lung cancer (SCLC) is characterized by prevalent circulating tumour cells (CTCs), early metastasis and poor prognosis. We show that SCLC patients (37/38) have rare CTC subpopulations co-expressing vascular endothelial-cadherin (VE-cadherin) and cytokeratins consistent with vasculogenic mimicry (VM), a process whereby tumour cells form ‘endothelial-like' vessels. Single-cell genomic analysis reveals characteristic SCLC genomic changes in both VE-cadherin-positive and -negative CTCs. Higher levels of VM are associated with worse overall survival in 41 limited-stage patients' biopsies (P<0.025). VM vessels are also observed in 9/10 CTC patient-derived explants (CDX), where molecular analysis of fractionated VE-cadherin-positive cells uncovered copy-number alterations and mutated TP53, confirming human tumour origin. VE-cadherin is required for VM in NCI-H446 SCLC xenografts, where VM decreases tumour latency and, despite increased cisplatin intra-tumour delivery, decreases cisplatin efficacy. The functional significance of VM in SCLC suggests VM regulation may provide new targets for therapeutic intervention.

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Section: Resultsmentioning

confidence: 56%

Section: Resultsmentioning

confidence: 93%

Vasculogenic mimicry in small cell lung cancer

et al. 2016

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“…Like in the case of angiogenesis, hypoxia promotes VM. In cell lines derived from esophageal carcinoma, it was observed that inhibition of HIF1alpha inhibits the formation of VM and decreases the levels of proteins involved in the creation of these vessels, such as VE-cadherin, EPHA2 (ephrin A2) and Laminin 5gamma2 (20,21). VE-cadherin is a relevant protein in VM.…”

Section: Vasculogenic Mimicry and Related Signal Pathwaysmentioning

confidence: 99%

An Overview of Vasculogenic Mimicry in Breast Cancer

et al. 2020

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Vasculogenic mimicry (VM) is the formation of vascular channels lacking endothelial cells. These channels are lined by tumor cells with cancer stem cell features, positive for periodic acid-Schiff, and negative for CD31 staining. The term VM was introduced by Maniotis et al. (1), who reported this phenomenon in highly aggressive uveal melanomas; since then, VM has been associated with poor prognosis, tumor aggressiveness, metastasis, and drug resistance in several tumors, including breast cancer. It is proposed that VM and angiogenesis (the de novo formation of blood vessels from the established vasculature by endothelial cells, which is observed in several tumors) rely on some common mechanisms. Furthermore, it is also suggested that VM could constitute a means to circumvent anti-angiogenic treatment in cancer. Therefore, it is important to determinant the factors that dictate the onset of VM. In this review, we describe the current understanding of VM formation in breast cancer, including specific signaling pathways, and cancer stem cells. In addition, we discuss the clinical significance of VM in prognosis and new opportunities of VM as a target for breast cancer therapy.

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“…VE-cadherin was also up-regulated by HIF-1α in esophageal carcinoma [18]. To summarize, hypoxia is an essential trigger for vascular signaling pathways in the process of vasculogenic mimicry.…”

Section: Ve-cadherin-dependent and Independent Signaling In Vmmentioning

confidence: 99%

Vasculogenic mimicry signaling revisited: focus on non-vascular VE-cadherin

et al. 2017

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Vasculogenic mimicry (VM) is a blood supply system independent of endothelial vessels in tumor cells from different origins. It reflects the plasticity of aggressive tumor cells that express vascular cell markers and line tumor vasculature. The presence of VM is associated with a high tumor grade, short survival, invasion and metastasis. Endothelial cells (ECs) express various members of the cadherin superfamily, in particular vascular endothelial (VE-) cadherin, which is the main adhesion receptor of endothelial adherent junctions. Aberrant extra-vascular expression of VE-cadherin has been observed in certain cancer types associated with VM. In this review we focus on non-endothelial VE-cadherin as a prominent factor involved in the acquisition of tubules-like structures by aggressive tumor cells and we summarize the specific signaling pathways, the association with trans-differentiation and stem-like phenotype and the therapeutic opportunities derived from the in-depth knowledge of the peculiarities of the biology of VE-cadherin and other key components of VM.

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HIF-1α induces VE-cadherin expression and modulates vasculogenic mimicry in esophageal carcinoma cells

Abstract: HIF-1α may modulate VM in ESCC by regulating VE-cadherin expression, which affects VM formation through EphA2 and LN5γ2.

Cited by 50 publications

References 36 publications

Vasculogenic mimicry in small cell lung cancer

Vasculogenic mimicry in small cell lung cancer

An Overview of Vasculogenic Mimicry in Breast Cancer

Vasculogenic mimicry signaling revisited: focus on non-vascular VE-cadherin

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