Endothelium originated from colorectal cancer stem cells constitute cancer blood vessels

Shangguan, Wenqi; Fan, Cheng; Chen, Xiaolong; Lu, Ran; Liu, Yuan; Yu, Li; Ya-zhen, Shang; Yin, Dongqin; Zhang, Shengliang; Huang, Qiaorong; Li, Xue; Wei, Meng; Xu, Hong; Zhou, Zong‐Guang; Hu, Jian-Kun; Mo, Xianming

doi:10.1111/cas.13262

Cited by 40 publications

(28 citation statements)

References 37 publications

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“…CRCSCs are able to initiate vascularization via pericytes by growth promotion (5,60). Thus, lack of pericytes recruitment impacts negatively in tumor size owing to poor vascular structure (61).…”

Section: Colorectal Cancermentioning

confidence: 99%

“…Conversely, TGFβ1/ALK5 pathway enhances angiogenesis by VEGF expression (66), being a critical signaling molecule for angiogenesis in CSCs (67). Moreover, VEGF-A/NRP-1 interaction promotes stemness properties in breast cancer (BC) cell lines by activation of Wnt/β-catenin pathway, since its inhibition relies in the attenuation of HUVEC-tube formation induced by co-culturing with extracts from Breast Cancer Stem Cells (BCSCs) (60). Moreover, glioblastoma stem-like cells (GSCs) produce VEGF-A, which is secreted in extracellular vesicles promoting permeability and angiogenesis in brain (68).…”

Section: Signaling Pathways Of Cscs In Angiogenesismentioning

confidence: 99%

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Cancer Stem Cells and Its Role in Angiogenesis and Vasculogenic Mimicry in Gastrointestinal Cancers

et al. 2020

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Cancer stem cells (CSCs) are able to promote initiation, survival and maintenance of tumor growth and have been involved in gastrointestinal cancers (GICs) such as esophageal, gastric and colorectal. It is well known that blood supply facilitates cancer progression, recurrence, and metastasis. In this regard, tumor-induced angiogenesis begins with expression of pro-angiogenic molecules such as vascular endothelial growth factor (VEGF), which in turn lead to neovascularization and thus to tumor growth. Another pattern of blood supply is called vasculogenic mimicry (VM). It is a reminiscent of the embryonic vascular network and is carried out by CSCs that have the capability of transdifferentiate and form vascular-tube structures in absence of endothelial cells. In this review, we discuss the role of CSCs in angiogenesis and VM, since these mechanisms represent a source of tumor nutrition, oxygenation, metabolic interchange and facilitate metastasis. Identification of CSCs mechanisms involved in angiogenesis and VM could help to address therapeutics for GICs.

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Section: Colorectal Cancermentioning

confidence: 99%

Section: Signaling Pathways Of Cscs In Angiogenesismentioning

confidence: 99%

Cancer Stem Cells and Its Role in Angiogenesis and Vasculogenic Mimicry in Gastrointestinal Cancers

et al. 2020

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“…In the same context, the accumulated data show that CSCs have the ability to differentiate into multi-lineage, such as pericytes, endothelial cells, and cancer-associated fibroblasts, and they have the potential to reconstruct their microenvironment by differentiation or recruitment of other cells and, therefore, contribute to the initiation and progression of cancers [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Hematopoietic Cells Derived from Cancer Stem Cells Generated from Mouse Induced Pluripotent Stem Cells

Hassan

Afify

Nair

et al. 2019

Cancers

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Cancer stem cells (CSCs) represent the subpopulation of cancer cells with the ability to differentiate into other cell phenotypes and initiated tumorigenesis. Previously, we reported generating CSCs from mouse induced pluripotent stem cells (miPSCs). Here, we investigated the ability of the CSCs to differentiate into hematopoietic cells. First, the primary cells were isolated from malignant tumors that were formed by the CSCs. Non-adherent cells (NACs) that arose from adherent cells were collected and their viability, as well as the morphology and expression of hematopoietic cell markers, were analyzed. Moreover, NACs were injected into the tail vein of busulfan conditioned Balb/c nude mice. Finally, CSCs were induced to differentiate to macrophages while using IL3 and SCF. The round nucleated NACs were found to be viable, positive for hematopoietic lineage markers and CD34, and expressed hematopoietic markers, just like homing to the bone marrow. When NACs were injected into mice, Wright-Giemsa staining showed that the number of white blood cells got higher than those in the control mice after four weeks. CSCs also showed the ability to differentiate toward macrophages. CSCs were demonstrated to have the potential to provide progenies with hematopoietic markers, morphology, and homing ability to the bone marrow, which could give new insight into the tumor microenvironment according to the plasticity of CSCs.

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“…Since Folkman proposed the anti-angiogenic therapy of tumor in 1971, a large number of studies have focused on the mechanisms of tumor vessel formation. Recent studies have paid attention to the generation of TECs, among which the endothelial trans-differentiation of CSCs has been demonstrated in glioblastoma and other malignancies (Tang et al, 2016;Shangguan et al, 2017;Cui et al, 2018). Several different regulatory factors, including Notch-1 (Cui et al, 2018) and CCL5 (Tang et al, 2016), are reportedly involved in the molecular mechanism of tumor-endothelial trans-differentiation.…”

Section: Discussionmentioning

confidence: 99%

Oct4 Regulates the Transition of Cancer Stem-Like Cells to Tumor Endothelial-Like Cells in Human Liver Cancer

Liu

Tang

Yang

et al. 2020

Front. Cell Dev. Biol.

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Octamer-binding transcription factor 4 (Oct4) has been recently implicated as a proangiogenic regulator in several induced pluripotent stem cells (iPSCs), however, its role in cancer stem-like cells (CSCs) remain unclear. We report here that Oct4 participates in tumor vasculogenesis in liver CSCs (LCSCs). We identify that LCSCs possess the potential of endothelial trans-differentiation under endothelial induction, present endothelial specific markers and their functions in vitro, and participate in neovasculogenesis in vivo. The knockdown of the Oct4A by short hairpin RNA (shRNA) in LCSCs represses endothelial trans-differentiation potential, but induces endothelial lineage-restricted differentiation, the latter is positively regulated by Oct4B1. Furthermore, Oct4 regulates vasculogenesis in LCSCs may be via the AKT-NF-κB-p65 signaling pathway. This work reveals Oct4, which is a crucial regulator, plays a critical role in tumor endothelial-like cells transition of LCSCs through Oct4A and Oct4B1 by different ways. The simultaneous inhibition of both the isoforms of Oct4 is hence expected to help regress neovascularization derived from CSCs. Our findings may provide insights to the possible new mechanisms of tumor vasculogenesis for primary liver cancer.

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Endothelium originated from colorectal cancer stem cells constitute cancer blood vessels

Cited by 40 publications

References 37 publications

Cancer Stem Cells and Its Role in Angiogenesis and Vasculogenic Mimicry in Gastrointestinal Cancers

Cancer Stem Cells and Its Role in Angiogenesis and Vasculogenic Mimicry in Gastrointestinal Cancers

Hematopoietic Cells Derived from Cancer Stem Cells Generated from Mouse Induced Pluripotent Stem Cells

Oct4 Regulates the Transition of Cancer Stem-Like Cells to Tumor Endothelial-Like Cells in Human Liver Cancer

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