Endothelial Cells (ECs) Metabolism: A Valuable Piece to Disentangle Cancer Biology

Lopes‐Coelho, Filipa; Martins, Filipa; Serpa, Jacinta

doi:10.1007/978-3-030-34025-4_8

Cited by 7 publications

(5 citation statements)

References 128 publications

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“…Studies have suggested that tumor angiogenesis results from the interaction of various cells and factors, including tumor cells and endothelial cells [ 14 , 15 ]. Immune cells, such as macrophages, are recruited and promote angiogenesis in the tumor microenvironment in some patients who are resistant to VEGF inhibitors [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Neutrophil extracellular traps promote angiogenesis in gastric cancer

Yang

Sun

et al. 2023

Cell Commun Signal

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Although antiangiogenic therapy has been used in gastric cancer, disease progression due to drug resistance remains common. Neutrophils play an important role in the occurrence and progression of cancer via neutrophil extracellular traps (NETs). However, few studies have investigated angiogenic regulation in gastric cancer. We aimed to determine the role of NETs in promoting angiogenesis in gastric cancer. Multiple immunohistochemical staining was used to analyze the spatial distribution of NETs and microvessels in patient tissue samples. A mouse subcutaneous tumor model was established to determine the effect of NETs on tumor growth, and changes in microvessel density were observed via immunohistochemical staining. We screened differentially expressed proteins in HUVECs stimulated by NETs via proteomics. Cell Counting Kit-8, EdU labeling, and tubule formation assays were used to verify the effect of NETs on HUVEC proliferation, migration, and tubule formation. Blocking NETs, which was related to decreased microvessel density, significantly inhibited tumor growth in the murine subcutaneous tumor model. Compared with those of the control group, tumor volume and mass among mice in the inhibition group decreased by 61.3% and 77.9%, respectively. The NET-DNA receptor CCDC25 was expressed in HUVECs, providing a platform for NETs to promote HUVEC proliferation, migration, and tubulation. In an in vitro rat aortic explant model, NETs induced HUVEC proliferation, survival, and chemotaxis, which were not significantly different from those observed in the VEGF stimulation group. Our results confirm that NETs promote angiogenesis in gastric cancer, providing a theoretical basis for identifying new anti-vascular therapeutic targets. Graphical Abstract

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Section: Introductionmentioning

confidence: 99%

Neutrophil extracellular traps promote angiogenesis in gastric cancer

Yang

Sun

et al. 2023

Cell Commun Signal

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“…Hypoxia, one of the hallmarks of TME, stimulates the production of pro-angiogenic factors by tumor cells, particularly vascular endothelial growth factor (VEGF), resulting in the activation of the “angiogenic switch” [ 38 ]. This triggers the proliferation and migration of ECs, leading to the formation of new blood vessels [ 39 ].…”

Section: Exploring the Role Of Ecs In The Tmementioning

confidence: 99%

Exploring the crosstalk between endothelial cells, immune cells, and immune checkpoints in the tumor microenvironment: new insights and therapeutic implications

Fang,

Lu,

Zheng

et al. 2023

Cell Death Dis

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The tumor microenvironment (TME) is a highly intricate milieu, comprising a multitude of components, including immune cells and stromal cells, that exert a profound influence on tumor initiation and progression. Within the TME, angiogenesis is predominantly orchestrated by endothelial cells (ECs), which foster the proliferation and metastasis of malignant cells. The interplay between tumor and immune cells with ECs is complex and can either bolster or hinder the immune system. Thus, a comprehensive understanding of the intricate crosstalk between ECs and immune cells is essential to advance the development of immunotherapeutic interventions. Despite recent progress, the underlying molecular mechanisms that govern the interplay between ECs and immune cells remain elusive. Nevertheless, the immunomodulatory function of ECs has emerged as a pivotal determinant of the immune response. In light of this, the study of the relationship between ECs and immune checkpoints has garnered considerable attention in the field of immunotherapy. By targeting specific molecular pathways and signaling molecules associated with ECs in the TME, novel immunotherapeutic strategies may be devised to enhance the efficacy of current treatments. In this vein, we sought to elucidate the relationship between ECs, immune cells, and immune checkpoints in the TME, with the ultimate goal of identifying novel therapeutic targets and charting new avenues for immunotherapy.

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“…Another glycolysis key enzyme is PFKFB3 and its blockage with the phosphatase inhibitor 3PO in endothelial cells resulted in tumor vessel normalization and impaired metastasis ( 53 , 211 ). This enzyme is usually overexpressed in cancer, and its inhibition with 1-(4-pyridinyl)-3-(2-quinolinyl)-2-propen-1-one (PFK15) blocked glycolysis and suppressed cell proliferation, motility and induced apoptosis of head and neck squamous cell carcinoma cells ( 212 ).…”

Section: From Primary Tumor To Metastasis: Metabolic Comparisonmentioning

confidence: 99%

Molecular and Metabolic Reprogramming: Pulling the Strings Toward Tumor Metastasis

et al. 2021

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Metastasis is a major hurdle to the efficient treatment of cancer, accounting for the great majority of cancer-related deaths. Although several studies have disclosed the detailed mechanisms underlying primary tumor formation, the emergence of metastatic disease remains poorly understood. This multistep process encompasses the dissemination of cancer cells to distant organs, followed by their adaptation to foreign microenvironments and establishment in secondary tumors. During the last decades, it was discovered that these events may be favored by particular metabolic patterns, which are dependent on reprogrammed signaling pathways in cancer cells while they acquire metastatic traits. In this review, we present current knowledge of molecular mechanisms that coordinate the crosstalk between metastatic signaling and cellular metabolism. The recent findings involving the contribution of crucial metabolic pathways involved in the bioenergetics and biosynthesis control in metastatic cells are summarized. Finally, we highlight new promising metabolism-based therapeutic strategies as a putative way of impairing metastasis.

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Endothelial Cells (ECs) Metabolism: A Valuable Piece to Disentangle Cancer Biology

Cited by 7 publications

References 128 publications

Neutrophil extracellular traps promote angiogenesis in gastric cancer

Neutrophil extracellular traps promote angiogenesis in gastric cancer

Exploring the crosstalk between endothelial cells, immune cells, and immune checkpoints in the tumor microenvironment: new insights and therapeutic implications

Molecular and Metabolic Reprogramming: Pulling the Strings Toward Tumor Metastasis

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