Identification of vascular cues contributing to cancer cell stemness and function

Kumar, Saran; Bar-Lev, Libat; Sharife, Husni; Grunewald, Myriam; Mogilevsky, Maxim; Licht, Tamar; Goveia, Jermaine; Taverna, Federico; Paldor, Iddo; Carmeliet, Peter

doi:10.1007/s10456-022-09830-z

Cited by 12 publications

(10 citation statements)

References 62 publications

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“…The bidirectional exchange of information between cancer and host cells contribute to acquisition of more aggressive phenotypes by the invading cancer cells (100X magnification, inset, white boarder, 400X). communication between vascular endothelial cells, macrophages, and CSC is central in orchestrating tumor progression (83,84).…”

Section: Cancer Stem Cells Vascular Endothelium and Tumor-associated ...mentioning

confidence: 99%

“…Bidirectional communication between CSC and host cells plays an essential role in augmenting the tumor-promoting functions of CSC. Recent studies suggest that bidirectional communication between vascular endothelial cells, macrophages, and CSC is central in orchestrating tumor progression ( 83 , 84 ).…”

Section: Cancer Stem Cells Vascular Endothelium and Tumor-associated ...mentioning

confidence: 99%

“…Vascular endothelial cells and macrophages extend the tumor promoting effect of CSC in several ways ( 83 – 85 ). In addition to their role in establishing a stem cell niche, endothelial cells provide essential nutrients to a rapidly growing population of tumor cells through their ability to amplify the blood supply to tumors on demand( 86 – 89 ).…”

Section: Cancer Stem Cells Vascular Endothelium and Tumor-associated ...mentioning

confidence: 99%

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Crosstalk between cancer stem cells and the tumor microenvironment drives progression of premalignant oral epithelium

Polverini

Nör²

2023

Front. Oral. Health

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Cancer stem cells (CSC) are a subpopulation of cancer cells that exhibit properties of self-renewal and differentiation and have been implicated in metastasis and treatment failures. There is mounting evidence that carcinogen-initiated mucosal epithelial stem cells acquire the CSC phenotype following exposure to environmental or infectious mutagens and are responsible for promoting the malignant transformation of premalignant (dysplastic) epithelium. CSC further contribute to the progression of dysplasia by activating signaling pathways through crosstalk with various cell populations in the tumor microenvironment. Two cell types, tumor-associated macrophages (TAM) and vascular endothelial cells (EC) nurture CSC development, support CSC stemness, and contribute to tumor progression. Despite mounting evidence implicating CSC in the initiation and progression of dysplastic oral epithelium to squamous cell carcinoma (SCC), the molecular mechanisms underlying these synergistic biological processes remain unclear. This review will examine the mechanisms that underlie the transformation of normal epithelial stem cells into CSC and the mechanistic link between CSC, TAM, and EC in the growth and the malignant conversation of dysplastic oral epithelium.

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Section: Cancer Stem Cells Vascular Endothelium and Tumor-associated ...mentioning

confidence: 99%

Section: Cancer Stem Cells Vascular Endothelium and Tumor-associated ...mentioning

confidence: 99%

Section: Cancer Stem Cells Vascular Endothelium and Tumor-associated ...mentioning

confidence: 99%

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Crosstalk between cancer stem cells and the tumor microenvironment drives progression of premalignant oral epithelium

Polverini

Nör²

2023

Front. Oral. Health

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“…Endothelial cells promote the GSC phenotype in the perivascular niche through direct cell–cell interactions by activating the Notch pathway in GSCs through the expression of Notch ligands and release of nitric oxide ( 34 – 37 ). Moreover, GSCs can secrete diffusible factors such as VEGF, which recruit tumor blood vessels to the niche ( 38 , 39 ). Other modalities of interactions between tumor cells and endothelial cells in GMB include microRNA-containing extracellular vesicles, gap junctions and non-coding RNAs ( 40 – 43 ).…”

Section: Vascularization Of Glioblastoma Multiformementioning

confidence: 99%

Vascular Co-Option and Other Alternative Modalities of Growth of Tumor Vasculature in Glioblastoma

Ribatti

2022

Front. Oncol.

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Non-angiogenic tumors grow in the absence of angiogenesis by two main mechanisms: cancer cells infiltrating and occupying the normal tissues to exploit pre-existing vessels (vascular co-option); the cancer cells themselves forms channels able to provide blood flow (the so called vasculogenic mimicry). In the original work on vascular co-option initiated by Francesco Pezzella, the non-angiogenic cancer cells were described as “exploiting” pre-existing vessels. Vascular co-option has been described in primary and secondary (metastatic) sites. Vascular co-option is defined as a process in which tumor cells interact with and exploit the pre-existing vasculature of the normal tissue in which they grow. As part of this process, cancer cells first migrate toward vessels of the primary tumor, or extravasate at a metastatic site and rest along the ab-luminal vascular surface. The second hallmark of vascular co-option is the interaction of cancer cells with the ab-luminal vascular surface. The first evidence for this was provided in a rat C6 glioblastoma model, showing that the initial tumor growth phase was not always avascular as these initial tumors can be vascularized by pre-existing vessels. The aim of this review article is to analyze together with vascular co-option, other alternative mode of vascularization occurring in glioblastoma multiforme (GBM), including vasculogenic mimicry, angiotropism and trans-differentiation of glioblastoma stem cells.

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“…Compared with normal blood vessels, the tumor vasculature is highly leaky, tortuous, and disorganized, which promotes solid tumor growth and metastasis [2] . Tumor blood vessels also contribute to the acquisition of cancer stem cell (CSC) characteristics [3] . More importantly, tumor blood vessels not only directly promote tumor growth and metastasis, they also play a role in immune escape.…”

Section: Introductionmentioning

confidence: 99%

Single-cell analysis of multiple cancer types reveals differences in endothelial cells between tumors and normal tissues

Zhang

Lü

et al. 2023

Computational and Structural Biotechnology Journal

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Identification of vascular cues contributing to cancer cell stemness and function

Cited by 12 publications

References 62 publications

Crosstalk between cancer stem cells and the tumor microenvironment drives progression of premalignant oral epithelium

Crosstalk between cancer stem cells and the tumor microenvironment drives progression of premalignant oral epithelium

Vascular Co-Option and Other Alternative Modalities of Growth of Tumor Vasculature in Glioblastoma

Single-cell analysis of multiple cancer types reveals differences in endothelial cells between tumors and normal tissues

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