The driving mechanism and targeting value of mimicry between vascular endothelial cells and tumor cells in tumor progression

Ma, Xiao; Geng, Ziang; Wang, Siqi; Yu, Zhuo; Liu, Tiancong; Guan, Sheng; Du, Shaonan; Zhu, Chen

doi:10.1016/j.biopha.2023.115029

Cited by 12 publications

(10 citation statements)

References 128 publications

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“…We previously identified TMEM230 as a master regulator of the sprouting of endothelial cells in vertebrate early development [5]. Additionally, we demonstrated that TMEM230 promotes vascular mimicry, a process generated by different cell types with microchannel formation capacity [2,5]. Microchannels formed during tissue wound healing are different from blood vessels formed in angiogenesis (Figure 1).…”

Section: Transmembrane Protein Tmem230 Expression Is Necessary For En...mentioning

confidence: 89%

“…Glial cells provide physical and chemical support for the homeostasis of the extracellular compartment of neural tissue through direct contacts and the secretion of soluble factors, vesicles, and insoluble and substrate-forming scaffolds [1]. Following injury, glial cells of the central nervous system promote tissue remodeling by microchanneling, new blood vessel formation, and scar formation, processes associated with normal wound healing [2][3][4]. Microchannel lumen structures, besides promoting passive permeability and the circulation of oxygen and nutrients, also allow for the diffusion of wound healing and angiogenesis-promoting factors (Figure 1).…”

Section: Introductionmentioning

confidence: 99%

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Transmembrane Protein TMEM230, Regulator of Glial Cell Vascular Mimicry and Endothelial Cell Angiogenesis in High-Grade Heterogeneous Infiltrating Gliomas and Glioblastoma

Cocola,

Abeni,

Martino

et al. 2024

IJMS

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High-grade gliomas (HGGs) and glioblastoma multiforme (GBM) are characterized by a heterogeneous and aggressive population of tissue-infiltrating cells that promote both destructive tissue remodeling and aberrant vascularization of the brain. The formation of defective and permeable blood vessels and microchannels and destructive tissue remodeling prevent efficient vascular delivery of pharmacological agents to tumor cells and are the significant reason why therapeutic chemotherapy and immunotherapy intervention are primarily ineffective. Vessel-forming endothelial cells and microchannel-forming glial cells that recapitulate vascular mimicry have both infiltration and destructive remodeling tissue capacities. The transmembrane protein TMEM230 (C20orf30) is a master regulator of infiltration, sprouting of endothelial cells, and microchannel formation of glial and phagocytic cells. A high level of TMEM230 expression was identified in patients with HGG, GBM, and U87-MG cells. In this study, we identified candidate genes and molecular pathways that support that aberrantly elevated levels of TMEM230 play an important role in regulating genes associated with the initial stages of cell infiltration and blood vessel and microchannel (also referred to as tumor microtubule) formation in the progression from low-grade to high-grade gliomas. As TMEM230 regulates infiltration, vascularization, and tissue destruction capacities of diverse cell types in the brain, TMEM230 is a promising cancer target for heterogeneous HGG tumors.

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Section: Transmembrane Protein Tmem230 Expression Is Necessary For En...mentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Transmembrane Protein TMEM230, Regulator of Glial Cell Vascular Mimicry and Endothelial Cell Angiogenesis in High-Grade Heterogeneous Infiltrating Gliomas and Glioblastoma

Cocola,

Abeni,

Martino

et al. 2024

IJMS

View full text Add to dashboard Cite

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“…In addition, endothelial cells undergo a process called endothelial-mesenchymal transition (EndMT), which results in the loss of their intercellular connections. Numerous potential targets and medications offer fresh perspectives and ideas for clinical targeted treatment and tumor immunotherapy [38] . In tumors, EndMT is an important source of cancer-related fibrous cells (CAFs) which are known to promote tumor progression in many ways [39] .…”

Section: Discussionmentioning

confidence: 99%

Integration of scRNA and bulk RNA-sequence to construct the 5-gene molecular prognostic model based on the heterogeneity of thyroid carcinoma endothelial cell

Ni,

Cong,

et al. 2024

ABBS

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Thyroid cancer (TC) is a kind of cancer with high heterogeneity, which leads to significant difference in prognosis. The prognostic molecular processes are not well understood. Cancer cells and tumor microenvironment (TME) cells jointly determine the heterogeneity. However, quite a little attention was paid to cells in the TME in the past years. In this study, we not only reveal that endothelial cells (ECs) are strongly associated with the progress of papillary thyroid cancer (PTC) using single-cell RNA-seq (scRNA-seq) data downloaded from Gene Expression Omnibus (GEO) and WGCNA, but also screen 5 crucial genes of ECs: CLDN5 , ABCG2 , NOTCH4 , PLAT , and TMEM47 . Furthermore, the 5-gene molecular prognostic model is constructed, which can predict how well a patient will do on PD-L1 blockade immunotherapy for TC and evaluate prognosis. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis demonstrates that PLAT is decreased in TC and the increase of PLAT can restrain the migratory capacity of TC cells. Meanwhile, in TC cells, PLAT suppresses VEGFa/VEGFR2-mediated human umbilical vascular endothelial cell (HUVEC) proliferation and tube formation. Totally, we construct the 5-gene molecular prognostic model from the perspective of EC and provide a new idea for immunotherapy of TC.

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“…Cytokine secretion by the VEGF family can effectively mediate multiple signaling pathways such as the paracrine signaling cascade, to orchestrate direct and indirect interactions between ECs and pericytes. This results in the regulation of cytokines, enzymes, and receptors such as TGF-β, MMP, and Tyrosine Kinase-2 (Tie2) receptors [ 80 , 81 , 82 ]. However, in tumor tissues the interactions between ECs and pericytes are defective, and this results in abnormalities in the structure, regulation and density of pericytes.…”

Section: Nanomedicines For Targeting Tme: Application Of Natural and ...mentioning

confidence: 99%

“…This contributes to increased heterogeneity on vasculature and triggers a hypoxic TME. Due to their dynamic characteristics and multiple molecular markers expression, pericytes in TME have a great potency to differentiate cancerous stromal fibroblasts that contribute to invasion and metastasis [ 80 , 81 , 82 ].…”

Section: Nanomedicines For Targeting Tme: Application Of Natural and ...mentioning

confidence: 99%

Biomaterial-Based Responsive Nanomedicines for Targeting Solid Tumor Microenvironments

Avgoustakis,

Angelopoulou

2024

Pharmaceutics

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Solid tumors are composed of a highly complex and heterogenic microenvironment, with increasing metabolic status. This environment plays a crucial role in the clinical therapeutic outcome of conventional treatments and innovative antitumor nanomedicines. Scientists have devoted great efforts to conquering the challenges of the tumor microenvironment (TME), in respect of effective drug accumulation and activity at the tumor site. The main focus is to overcome the obstacles of abnormal vasculature, dense stroma, extracellular matrix, hypoxia, and pH gradient acidosis. In this endeavor, nanomedicines that are targeting distinct features of TME have flourished; these aim to increase site specificity and achieve deep tumor penetration. Recently, research efforts have focused on the immune reprograming of TME in order to promote suppression of cancer stem cells and prevention of metastasis. Thereby, several nanomedicine therapeutics which have shown promise in preclinical studies have entered clinical trials or are already in clinical practice. Various novel strategies were employed in preclinical studies and clinical trials. Among them, nanomedicines based on biomaterials show great promise in improving the therapeutic efficacy, reducing side effects, and promoting synergistic activity for TME responsive targeting. In this review, we focused on the targeting mechanisms of nanomedicines in response to the microenvironment of solid tumors. We describe responsive nanomedicines which take advantage of biomaterials’ properties to exploit the features of TME or overcome the obstacles posed by TME. The development of such systems has significantly advanced the application of biomaterials in combinational therapies and in immunotherapies for improved anticancer effectiveness.

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The driving mechanism and targeting value of mimicry between vascular endothelial cells and tumor cells in tumor progression

Cited by 12 publications

References 128 publications

Transmembrane Protein TMEM230, Regulator of Glial Cell Vascular Mimicry and Endothelial Cell Angiogenesis in High-Grade Heterogeneous Infiltrating Gliomas and Glioblastoma

Transmembrane Protein TMEM230, Regulator of Glial Cell Vascular Mimicry and Endothelial Cell Angiogenesis in High-Grade Heterogeneous Infiltrating Gliomas and Glioblastoma

Integration of scRNA and bulk RNA-sequence to construct the 5-gene molecular prognostic model based on the heterogeneity of thyroid carcinoma endothelial cell

Biomaterial-Based Responsive Nanomedicines for Targeting Solid Tumor Microenvironments

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