A novel monoclonal antibody targeting a novel epitope of VE‑cadherin inhibits vasculogenic mimicry of lung cancer cells

Ding, Jie; Jia, Xi; Zuo, Bin; He, Jun; Yang, Jianfeng; He, Yang

doi:10.3892/or.2018.6374

Cited by 10 publications

(10 citation statements)

References 20 publications

(22 reference statements)

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“…This antibody targets the outer-membrane immunoglobulin-like domains of VE-cadherin, blocking receptor function. In lung cancer cells, it was observed that this antibody functions as an anti-VM agent for cancer treatment, since it inhibited the activation of the VE-cadherin-related pathway in VM (182). Due to the advantages that monoclonal antibody therapies imply, its application in ovarian cancer as an anti-VM agent is promising.…”

Section: Clinical Implications Of the Signaling Molecules Of Vm In Ovmentioning

confidence: 99%

Mechanisms of Vasculogenic Mimicry in Ovarian Cancer

et al. 2019

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Solid tumors carry out the formation of new vessels providing blood supply for growth, tumor maintenance, and metastasis. Several processes take place during tumor vascularization. In angiogenesis, new vessels are derived from endothelial cells of pre-existing vessels; while in vasculogenesis, new vessels are formed de novo from endothelial progenitor cells, creating an abnormal, immature, and disorganized vascular network. Moreover, highly aggressive tumor cells form structures similar to vessels, providing a pathway for perfusion; this process is named vasculogenic mimicry (VM), where vessel-like channels mimic the function of vessels and transport plasma and blood cells. VM is developed by numerous types of aggressive tumors, including ovarian carcinoma which is the second most common cause of death among gynecological cancers. VM has been associated with poor patient outcome and survival in ovarian cancer, although the involved mechanisms are still under investigation. Several signaling molecules have an important role in VM in ovarian cancer, by regulating the expression of genes related to vascular, embryogenic, and hypoxic signaling pathways. In this review, we provide an overview of the current knowledge of the signaling molecules involved in the promotion and regulation of VM in ovarian cancer. The clinical implications and the potential benefit of identification and targeting of VM related molecules for ovarian cancer treatment are also discussed.

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Section: Clinical Implications Of the Signaling Molecules Of Vm In Ovmentioning

confidence: 99%

Mechanisms of Vasculogenic Mimicry in Ovarian Cancer

et al. 2019

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“…First discovered in uveal melanoma in 1999 [20], during the following 20 years, VM has been reported in several malignant tumours, including melanoma [22,23], glioblastoma [24,25], osteosarcoma [26,27], hepatocellular carcinoma [28,29], and breast [30,31], lung [32,33], gastric [19,34], colorectal [35,36] and prostate [37,38] cancers. VM is associated with a high tumour grade, invasion, metastasis and poor prognosis in patients with malignant tumours [39][40][41][42][43], including breast [44], colorectal [36], prostate [45], hepatocellular [46], lung [45], ovarian [47], gastric [48] and bladder [49] cancers. To date, the precise mechanisms underlying VM formation are still under investigation; what is known is its correlation with ECM remodelling, certain tumour environmental conditions, and a dedifferentiated state proper of stem-like cells or cancer stem cells (CSCs).…”

Section: Introductionmentioning

confidence: 99%

Physicochemical aspects of the tumour microenvironment as drivers of vasculogenic mimicry

Andreucci

Peppicelli

Ruzzolini

et al. 2022

Cancer Metastasis Rev

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Tumour vascularisation is vital for cancer sustainment representing not only the main source of nutrients and oxygen supply but also an escape route for single or clustered cancer cells that, once detached from the primary mass, enter the blood circulation and disseminate to distant organs. Among the mechanisms identified to contribute to tumour vascularisation, vasculogenic mimicry (VM) is gaining increasing interest in the scientific community representing an intriguing target for cancer treatment. VM indeed associates with highly aggressive tumour phenotypes and strongly impairs patient outcomes. Differently from vessels of healthy tissues, tumour vasculature is extremely heterogeneous and tortuous, impeding efficient chemotherapy delivery, and at the meantime hyperpermeable and thus extremely accessible to metastasising cancer cells. Moreover, tumour vessel disorganisation creates a self-reinforcing vicious circle fuelling cancer malignancy and progression. Because of the inefficient oxygen delivery and metabolic waste removal from tumour vessels, many cells within the tumour mass indeed experience hypoxia and acidosis, now considered hallmarks of cancer. Being strong inducers of vascularisation, therapy resistance, inflammation and metastasis, hypoxia and acidosis create a permissive microenvironment for cancer progression and dissemination. Along with these considerations, we decided to focus our attention on the relationship between hypoxia/acidosis and VM. Indeed, besides tumour angiogenesis, VM is strongly influenced by both hypoxia and acidosis, which could potentiate each other and fuel this vicious circle. Thus, targeting hypoxia and acidosis may represent a potential target to treat VM to impair tumour perfusion and cancer cell sustainment.

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“…Accumulating evidence suggests that VM is associated with poor prognosis in various malignant human tumors, including breast [27], colorectal [28], prostate [29], hepatocellular carcinoma [30], lung [29], ovarian [31], gastric [32], and bladder cancers [33]. Despite numerous experimental studies, the prognostic value of VM status for survival in MM patients is still controversial and inconclusive.…”

Section: Introductionmentioning

confidence: 99%

The role of vascular mimicry as a biomarker in malignant melanoma: a systematic review and meta-analysis

et al. 2019

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BackgroundVasculogenic mimicry (VM) a microvascular system consisting of non-endothelial cells that is newly formed by aggressive tumors, has been proposed as an important therapeutic target in malignant melanoma (MM). We performed a systematic literature review to evaluate the diagnostic and prognostic accuracy of VM status for overall survival of MM patients.MethodsThe quality of the included studies was evaluated using the QUADAS-2 tool. Diagnostic capacity of VM variables, including sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and the area under summary receiver operating characteristic (SROC), were pooled using Meta-DiSc software.ResultsA retrospective observational study was conducted based on twelve clinical studies including 978 clinically confirmed melanoma patients with proportion (P). VM+ melanoma cells were associated with poor prognosis in 38% of MM group (P = 0.35, 95% confidence intervals (CI): 0.27–0.42, p < 0.001). The pooled sensitivity and specificity were 0.82 (95% CI: 0.79–0.84) and 0.69 (95% CI: 0.66–0.71), respectively. Furthermore, the pooled PLR, NLR, and DOR were 2.56 (95% CI: 1.94–3.93), 0.17 (95% CI: 0.07–0.42), and 17.75 (95% CI: 5.30–59.44), respectively. Furthermore, the AUC of SROC was 0.63, indicating high reliability of VM status as a biomarker. Importantly, subgroup results suggested that VM+ status is a significantly accurate prognostic biomarker when diagnosed by the CD31−/PAS+ staining methods in Asian MM samples (p < 0.001).ConclusionsOur findings support the potential of VM status of tumors as a promising prognostic biomarker and emphasize an effective adjuvant therapeutic strategy in the prognosis of Asian MM patients.

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A novel monoclonal antibody targeting a novel epitope of VE‑cadherin inhibits vasculogenic mimicry of lung cancer cells

Cited by 10 publications

References 20 publications

Mechanisms of Vasculogenic Mimicry in Ovarian Cancer

Mechanisms of Vasculogenic Mimicry in Ovarian Cancer

Physicochemical aspects of the tumour microenvironment as drivers of vasculogenic mimicry

The role of vascular mimicry as a biomarker in malignant melanoma: a systematic review and meta-analysis

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