The relationship between vasculogenic mimicry and epithelial‐mesenchymal transitions

Liu, Qiqi; Qiao, Lili; Liang, Ning; Xie, Jian; Zhang, Jingxin; Deng, Guohua; Luo, Hui; Zhang, Jiandong

doi:10.1111/jcmm.12851

Cited by 101 publications

(101 citation statements)

References 83 publications

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“…Recent studies have shown that EMT, in which the cell‐cell junction is lost and cells lose the epithelial phenotype and acquire mesenchymal features, is a critical step in the process of cancer metastasis . Additionally, EMT plays a crucial role in VM formation . In our study, we tested whether EMT participates in the inhibition of VM formation by TP53INP1.…”

Section: Discussionmentioning

confidence: 96%

TP53INP1 inhibits hypoxia‐induced vasculogenic mimicry formation via the ROS/snail signalling axis in breast cancer

Wang

Sun

Zhang

et al. 2018

J Cellular Molecular Medi

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Tumour protein p53‐inducible nuclear protein 1 (TP53INP1) is a tumour suppressor associated with malignant tumour metastasis. Vasculogenic mimicry (VM) is a new tumour vascular supply pattern that significantly influences tumour metastasis and contributes to a poor prognosis. However, the molecular mechanism of the relationship between TP53INP1 and breast cancer VM formation is unknown. Here, we explored the underlying mechanism by which TP53INP1 regulates VM formation in vitro and in vivo. High TP53INP1 expression was not only negatively correlated with a poor prognosis but also had a negative relationship with VE‐cadherin, HIF‐1α and Snail expression. TP53INP1 overexpression inhibited breast cancer invasion, migration, epithelial‐mesenchymal transition (EMT) and VM formation; conversely, TP53INP1 down‐regulation promoted these processes in vitro by functional experiments and Western blot analysis. We established a hypoxia model induced by CoCl2 and assessed the effects of TP53INP1 on hypoxia‐induced EMT and VM formation. In addition, we confirmed that a reactive oxygen species (ROS)‐mediated signalling pathway participated in TP53INP1‐mediated VM formation. Together, our results show that TP53INP1 inhibits hypoxia‐induced EMT and VM formation via the ROS/GSK‐3β/Snail pathway in breast cancer, which offers new insights into breast cancer clinical therapy.

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Section: Discussionmentioning

confidence: 96%

TP53INP1 inhibits hypoxia‐induced vasculogenic mimicry formation via the ROS/snail signalling axis in breast cancer

Wang

Sun

Zhang

et al. 2018

J Cellular Molecular Medi

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“…Recently, many studies have proposed that EMT is vital for VM formation and tumor progression (9). Some regulatory factors, such as Twist, Runx2 and ZEB2, play important roles in VM formation by promoting EMT (6,16,17).…”

Section: Discussionmentioning

confidence: 99%

“…EMT is regulated by many transcription factors, including the traditional factor ZEB1. The role of EMT in the development of VM has recently attracted attention (9,15,16). Liu et al (8) confirmed that ZEB1 can promote VM formation by inducing EMT in colorectal cancer.…”

Section: Vasculogenic Mimicry In Bladder Cancer and Its Association Wmentioning

confidence: 99%

“…The phenomenon has been observed in many tumor types, including hepatocellular carcinoma, breast, colorectal and prostate cancer (5)(6)(7)(8). Numerous studies (8)(9)(10) have shown that the existence of VM is closely related to the invasion, metastasis and poor prognosis of malignant tumors, which is significant in the clinic. At present, the literature about VM in bladder cancer, particularly its molecular mechanism, is very limited.…”

Section: Introductionmentioning

confidence: 99%

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Vasculogenic mimicry in bladder cancer and its association with the aberrant expression of ZEB1

Mao

Wang

et al. 2018

Oncol Lett

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Abstract. The aim of the present study was to investigate the associations between vasculogenic mimicry (VM) and zinc finger E-box binding homeobox 1 (ZEB1) in bladder cancer. VM structure and ZEB1 expression were analyzed by cluster of differentiation 34/periodic acid Schiff (PAS) double staining and immunohistochemical staining in 135 specimens from patients with bladder cancer, and a further 12 specimens from normal bladder tissues. Three-dimensional (3-D) culture was used to detect VM formation in the bladder transitional cancer cell lines UM-UC-3 and J82, and the immortalized human bladder epithelium cell line SV-HUC-1 in vitro. ZEB1 expression in these cell lines was compared by reverse transcription-quantitative polymerase chain reaction and western blot assays. In addition, small interfering RNA was used to inhibit ZEB1 in UM-UC-3 and J82 cells, followed by 3-D culturing of treated cell lines. As a result, VM was observed in 31.1% of specimens from bladder cancer tissues, and cases with high ZEB1 expression accounted for 60.0% of patients with bladder cancer. In addition, ZEB1 expression was closely associated with VM (r=0.189; P<0.05), and also increased as the grade and stage of the tumor developed. In an in vitro assay, UM-UC-3 and J82 cells exhibited VM formation, however, SV-HUC-1 did not. Furthermore, VM-forming cancer cell lines UM-UC-3 and J82 exhibited higher ZEB1 expression. Notably, VM formation was inhibited following knockdown of ZEB1. In conclusion, ZEB1 may be associated with VM in bladder cancer and serve an important role in the process of VM formation. However, its detailed mechanism requires further study.

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“…Further evidences have found that EMT regulators and EMT-related transcription factors are highly upregulated in VM-forming tumor cells 27. Many studies have demonstrated that adhesion molecules and other factors modulating EMT process can regulate VM formation, such as Twist, ZEB1, Snail, and Slug/Snail2 14. In this study, we performed an IHC stain of E-cadherin, a well-established indicator of EMT, and discovered that VM was associated with EMT.…”

Section: Discussionmentioning

confidence: 79%

Vasculogenic mimicry is associated with increased tumor-infiltrating neutrophil and poor outcome in esophageal squamous cell carcinoma

Zhang

Deng

et al. 2017

OTT

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PurposeVasculogenic mimicry (VM) is known to be a mechanism to nourish the tumor, but little is known about its prognostic significance in esophageal squamous cell carcinoma (ESCC). We characterized the predictive relevance of VM expression and tumor-infiltrating neutrophil (TIN) density in patients with resectable ESCC.MethodsWe retrospectively collected clinicopathologic characteristics of 117 esophageal cancer (EC) patients undergoing complete resection and without preoperative therapy. Immunohistochemistry was used to detect the expression of E-cadherin and CD66b. CD34/periodic acid-schiff (PAS) double staining was used to detect the expression of VM.ResultsVM expression was observed in 56 (47.9%) patients. VM was negatively correlated with E-cadherin (correlation coefficient =−0.364, P<0.001) and was positively correlated with infiltration of CD66b neutrophil (correlation coefficient =0.421, P<0.001). VM and CD66b+ neutrophil infiltration are important markers for poor overall survival and disease-free survival. Multivariate analysis showed that VM, CD66b+ neutrophil infiltration, pathologic tumor node metastasis (TNM) (pTNM) stage, and tumor differentiation are significant independent prognostic predictors in ECs (P=0.001, 0.025, 0.001, 0.011, respectively). VM expression is identified in ~47.9% of ESCC, and it is associated with poor outcome and increased TIN.ConclusionTIN is an important factor for VM formation. Therefore, studies of invasive ability of EC in patients with VM could supply significant information for therapeutic strategy.

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The relationship between vasculogenic mimicry and epithelial‐mesenchymal transitions

Cited by 101 publications

References 83 publications

TP53INP1 inhibits hypoxia‐induced vasculogenic mimicry formation via the ROS/snail signalling axis in breast cancer

TP53INP1 inhibits hypoxia‐induced vasculogenic mimicry formation via the ROS/snail signalling axis in breast cancer

Vasculogenic mimicry in bladder cancer and its association with the aberrant expression of ZEB1

Vasculogenic mimicry is associated with increased tumor-infiltrating neutrophil and poor outcome in esophageal squamous cell carcinoma

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