The Role of YAP and TAZ in Angiogenesis and Vascular Mimicry

Azad, Taha; Ghahremani, Mina; Yang, Xiaolong

doi:10.3390/cells8050407

Cited by 82 publications

(77 citation statements)

References 145 publications

(163 reference statements)

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“…Angiogenesis can be divided in two types: sprouting and intussusceptive (48)(49)(50). In the first one, ECs proliferate and sprout toward an angiogenic stimulator (e.g., VEGF), forming flat structures called filopodia, producing proteolytic enzymes to enhance angiogenic process (51).…”

Section: Promotion Of Angiogenesis By Gastrointestinal Cscsmentioning

confidence: 99%

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: Promotion Of Angiogenesis By Gastrointestinal Cscsmentioning

confidence: 99%

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

et al. 2020

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“…Other research teams have therefore carried on studying the roles of the Hippo pathway in angiogenesis, starting with proteins belonging to the AMOT family: AMOT, AMOTL1, AMOTL2. These proteins regulate endothelial cell motility and are both known to interact with YAP and to be transcriptional targets of YAP/TEAD complex [38][39][40][41][42].…”

Section: Angiogenesismentioning

confidence: 99%

Hippo/YAP Signaling Pathway: A Promising Therapeutic Target in Bone Paediatric Cancers?

Morice

Danieau

Rédini

et al. 2020

Cancers

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Osteosarcoma and Ewing sarcoma are the most prevalent bone pediatric tumors. Despite intensive basic and medical research studies to discover new therapeutics and to improve current treatments, almost 40% of osteosarcoma and Ewing sarcoma patients succumb to the disease. Patients with poor prognosis are related to either the presence of metastases at diagnosis or resistance to chemotherapy. Over the past ten years, considerable interest for the Hippo/YAP signaling pathway has taken place within the cancer research community. This signaling pathway operates at different steps of tumor progression: Primary tumor growth, angiogenesis, epithelial to mesenchymal transition, and metastatic dissemination. This review discusses the current knowledge about the involvement of the Hippo signaling pathway in cancer and specifically in paediatric bone sarcoma progression.

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“…20 When macrophage stimulating (Mst) 1/2 is activated by activation of Hippo signaling, Mstl/2 kinase and the scaffolding protein Savl form the complex that phosphorylates and activates Lats1/2 (Large tumor suppressor; LATS) kinase. 21 Further, phosphorylated Lats1/2 is in combination with the scaffolding protein Mobl forms complex that phosphorylate YAP. Phosphorylation of S127 of YAP produces a 14-3-3 binding motif, leading to its retention cytoplasm through binding with the intracytoplasmic 14-3-3 proteins, resulting in decreased nuclear entry of YAP or further was phosphorylation by the proteasome pathway.…”

Section: Dovepressmentioning

confidence: 99%

“…Thus, YAP enters the non-phosphorylated state of the nucleus in an unphosphorylated state to bind to other transcription factors and exerts its biological effects. 21 Intranuclear YAP binds to the transcription factor TEAD (TEA-domain) and promotes or represses the expression of TEAD target gene expression, including Cyr61, CTGF, and Birc5, thereby regulating various biological functions, such as cell growth, cell contact inhibition, control of tissue and organ size, and self-renewal of stem cells. 22 Overexpressed YAP binds to TEAD thereby inhibiting activating the activation through the Hippo signaling pathway.…”

Section: Dovepressmentioning

confidence: 99%

<p>SRPX2 Promotes Cell Proliferation and Invasion in Osteosarcoma Through Regulating Hippo Signaling Pathway</p>

Wu¹,

Wang²,

Chen³

et al. 2020

OTT

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Background/Purpose: Osteosarcoma (OS), a primary bone malignancy, is characterized by a high rate of metastasis. It has been found that Sushi repeat containing protein X-linked 2 (SRPX2) is involved in tumor cell proliferation, adhesion, invasion and migration. The current work aimed to explore the effect of SRPX2 on OS cell invasion and proliferation. Methods: Immunohistochemistry (IHC), Western blotting and reverse transcriptionpolymerase chain reaction (RT-PCR) were used to detect the expression of the associated protein in OS tissues and cell lines. Cell counting kit-8 (CCK8), transwell and colony formation assays were used to determine cell viability, invasion, and proliferation, respectively. The in vivo tumorigenic ability of SRPX2 gene was determined using nude mouse tumorigenesis test. Results: SRPX2 knockdown suppressed the viability, while SRPX2 overexpression increased the invasion and colony formation ability of the cells in vitro. In vivo experiments demonstrated that SRPX2 knockdown inhibited tumor growth and invasion as evidenced by decreased Ki67 and N-cadherin levels, and increased E-cadherin level. Downregulation of SRPX2 increased YAP phosphorylation resulting in reduced nuclear translocation to activate Hippo signaling pathway. The promotion of cell viability, colony-forming ability, and invasion, and the inhibition of CTGF, Cyr61, and Birc5 levels promoted by SRPX2 overexpression were reversed by YAP inhibition. Conclusion: SRPX2 increased cell proliferation and invasion in osteosarcoma by activating Hippo signaling pathway.

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The Role of YAP and TAZ in Angiogenesis and Vascular Mimicry

Cited by 82 publications

References 145 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

Hippo/YAP Signaling Pathway: A Promising Therapeutic Target in Bone Paediatric Cancers?

<p>SRPX2 Promotes Cell Proliferation and Invasion in Osteosarcoma Through Regulating Hippo Signaling Pathway</p>

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