An Overview of Vasculogenic Mimicry in Breast Cancer

Andonegui-Elguera, Marco A.; Alfaro-Mora, Yair; Cáceres-Gutiérrez, Rodrigo E.; Caro-Sánchez, Claudia Haydeé Saraí; Herrera, Luis A.; Díaz‐Chávez, José

doi:10.3389/fonc.2020.00220

Cited by 65 publications

(48 citation statements)

References 73 publications

(83 reference statements)

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“…Although their existence has been controversially discussed for the last two decades, VM vessels occur in a variety of solid tumors with a bad prognosis for the patient (Andonegui-Elguera et al, 2020;Wechman et al, 2020;Wei et al, 2021). These vessels are hardly or not at all lined by endothelial cells, but possess a sleeve of ECM glycoproteins.…”

Section: The Prothrombotic Microenvironment Of Solid Tumorsmentioning

confidence: 99%

Platelets, Constant and Cooperative Companions of Sessile and Disseminating Tumor Cells, Crucially Contribute to the Tumor Microenvironment

Obermann

Brockhaus

Eble

2021

Front. Cell Dev. Biol.

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Although platelets and the coagulation factors are components of the blood system, they become part of and contribute to the tumor microenvironment (TME) not only within a solid tumor mass, but also within a hematogenous micrometastasis on its way through the blood stream to the metastatic niche. The latter basically consists of blood-borne cancer cells which are in close association with platelets. At the site of the primary tumor, the blood components reach the TME via leaky blood vessels, whose permeability is increased by tumor-secreted growth factors, by incomplete angiogenic sprouts or by vasculogenic mimicry (VM) vessels. As a consequence, platelets reach the primary tumor via several cell adhesion molecules (CAMs). Moreover, clotting factor VII from the blood associates with tissue factor (TF) that is abundantly expressed on cancer cells. This extrinsic tenase complex turns on the coagulation cascade, which encompasses the activation of thrombin and conversion of soluble fibrinogen into insoluble fibrin. The presence of platelets and their release of growth factors, as well as fibrin deposition changes the TME of a solid tumor mass substantially, thereby promoting tumor progression. Disseminating cancer cells that circulate in the blood stream also recruit platelets, primarily by direct cell-cell interactions via different receptor-counterreceptor pairs and indirectly by fibrin, which bridges the two cell types via different integrin receptors. These tumor cell-platelet aggregates are hematogenous micrometastases, in which platelets and fibrin constitute a particular TME in favor of the cancer cells. Even at the distant site of settlement, the accompanying platelets help the tumor cell to attach and to grow into metastases. Understanding the close liaison of cancer cells with platelets and coagulation factors that change the TME during tumor progression and spreading will help to curb different steps of the metastatic cascade and may help to reduce tumor-induced thrombosis.

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Section: The Prothrombotic Microenvironment Of Solid Tumorsmentioning

confidence: 99%

Platelets, Constant and Cooperative Companions of Sessile and Disseminating Tumor Cells, Crucially Contribute to the Tumor Microenvironment

Obermann

Brockhaus

Eble

2021

Front. Cell Dev. Biol.

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“…Excepting endothelium mediated angiogenesis, a novel type of tumour vessel supply called vasculogenic mimicry (VM), which is created by c tumour cells and the extracellular matrix, has been found 9,10 . VM may be the key reason for the ineffectiveness of existing antiangiogenic agents 11 .…”

Section: Introductionmentioning

confidence: 99%

Salvianolic acid A blocks vasculogenic mimicry formation in human non‐small cell lung cancer via PI3K/Akt/mTOR signalling

Jin

Chen

Huang

et al. 2021

Clin Exp Pharma Physio

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Vasculogenic mimicry (VM) is associated with aggressive cancer cells. Salvianolic acid A (Sal‐A), an antioxidant and anti‐inflammatory agent, has bioactive properties from Salvia miltiorrhiza Bunge. Current investigation aspired to explore the activity of Sal‐A in the VM formation of non‐small cell lung cancer (NSCLC) and the mechanism underling this function. The CCK8, the scratch and boyden chemotaxis assay were presented to describe NSCLC cells viability, migration and invasion capabilities, respectively. The protein expression was verified by western blotting. In this report, Sal‐A caused a reduction in viability, metastasis and capillaries structure formation of NSCLC cells. Additionally, Sal‐A markedly prevented the key VM related proteins, containing EphA2, VE‐cadherin and MMP2. Besides, Sal‐A significantly diminished p‐PI3K, p‐Akt and p‐mTOR level in NSCLC cells. More importantly, SC79 pretreatment reversed Sal‐A inhibits NSCLC cells viability, metastasis and VM formation. These data exhibit that Sal‐A could block VM network formation in NSCLC cells through modulating the PI3K/Akt/mTOR signalling pathway.

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“…What can be confirmed is that hypoxia induces vasculogenic mimicry (VM) 48 and the latter is vascular endothelial cell independent perfusion way. VM compensated the function of angiogenesis and represents greater invasiveness and poorer prognosis 49 . VM, plus chemo-resist stem cells 50 and clonal evolution 44 , makes Bev a double-edged sword in treating BC.…”

Section: Discussionmentioning

confidence: 99%

Bevacizumab Plays a double-edged role in Neoadjuvant Therapy for Non-metastatic Breast Cancer: A Systemic Review and Meta-Analysis

Chen¹,

Gao²,

Zhang³

et al. 2021

J. Cancer

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The anti-angiogenic drug Bevacizumab (Bev) is engaged in neoadjuvant therapy for non-metastatic breast cancer (NMBC). However, whether neoadjuvant Bev providing a greater benefit to patients is debatable. Our study aimed to review Bev's role in Neoadjuvant therapy (NAT) in NMBC and identify predictive markers associated with its efficacy by systemic review and meta-analysis. Eligible trials were retrieved from the Pubmed, Embase, and Cochrane Library, and random or fixed effects models were applied to synthesize data. Power of pCR to predict DFS or OS was evaluated by nonlinear mixed effect model. In NMBC, Bev significantly improved the rate of patients achieving pCR, but this benefit discontinued in DFS or OS. Biomarkers such as PAM50 intrinsic subtype, VEGF overexpression, regulation of VEGF signaling pathway, hypoxia-related genes, BRCA1/2 mutation, P53 mutation and immune phenotype can be used to predict Bev-inducing pCR and/or DFS/OS. Unfortunately, although patients with pCR survived longer than those without pCR when ignoring the use of Bev, but patients achieving pCR with Bev might survive shorter than those achieving pCR without Bev. Subgroup analyses found Bev prolonged patients' OS when given pre-and post-surgery. Lastly, adding Bev increased adverse effects. Overall, Bev offered limited effect for patients with NMBC in an unscreened population. However, in biomarkers-identified subgroup, Bev could be promising to ameliorate the prognosis of specific patients with NMBC.

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An Overview of Vasculogenic Mimicry in Breast Cancer

Cited by 65 publications

References 73 publications

Platelets, Constant and Cooperative Companions of Sessile and Disseminating Tumor Cells, Crucially Contribute to the Tumor Microenvironment

Platelets, Constant and Cooperative Companions of Sessile and Disseminating Tumor Cells, Crucially Contribute to the Tumor Microenvironment

Salvianolic acid A blocks vasculogenic mimicry formation in human non‐small cell lung cancer via PI3K/Akt/mTOR signalling

Bevacizumab Plays a double-edged role in Neoadjuvant Therapy for Non-metastatic Breast Cancer: A Systemic Review and Meta-Analysis

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