Role of Cytokines and Chemokines in Angiogenesis in a Tumor Context

Geindreau, Mannon; Bruchard, Mélanie; Végran, Frédérique

doi:10.3390/cancers14102446

Cited by 58 publications

(41 citation statements)

References 161 publications

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“…Among the important factors for HCC development are angiogenesis and signaling cascades for regulating cell proliferation such as the Raf/MAPK kinase/MAPK pathway, which is activated in numerous hepatic carcinoma derived cell lines and tumor samples 3 . Tumor angiogenesis is induced by an increased secretion of endogenous angiogenic factors or down-regulation of angiogenesis inhibitors 4 , 5 . Angiogenic factors are produced by tumor cells and by other cell types such as: endothelial cells, fibroblasts, smooth muscle cells/pericytes, and infiltrating immune cells; they initiate the angiogenic process by activating endothelial cells and induction of the angiogenic switch 4 , 6 .…”

Section: Introductionmentioning

confidence: 99%

Ramucirumab combination with sorafenib enhances the inhibitory effect of sorafenib on HepG2 cancer cells

Taha

Aboulwafa

Zedan

et al. 2022

Sci Rep

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Sorafenib, an oral multiple kinase inhibitor, is the standardized treatment for hepatocellular carcinoma (HCC). One strategy to improve HCC therapy is to combine agents that target key signaling pathways. In this study we set out to investigate the effect of combining sorafenib with either bevacizumab (anti-VEGF), panitumumab (anti-EGFR) or ramucirumab (anti-VEGFR2) on HepG2 cancer cell line with the aim of improving efficacy and possibility of therapeutic dose reduction of sorafenib.: HepG2 cancer cell line was treated with sorafenib alone or in combination with either bevacizumab, panitumumab or ramucirumab. Cell proliferation; apoptosis and cell cycle distribution; gene expression of VEGFR2, EGFR, MMP-9 and CASPASE3; the protein levels of pVEGFR2 and pSTAT3 and the protein expression of CASPASE3, EGFR and VEGFR2 were determined. Combined treatments of sorafenib with ramucirumab or panitumumab resulted in a significant decrease in sorafenib IC50. Sorafenib combination with ramucirumab or bevacizumab resulted in a significant arrest in pre-G and G0/G1 cell cycle phases, significantly induced apoptosis and increased the relative expression of CASPASE3 and decreased the anti-proliferative and angiogenesis markers´ MMP-9 and pVEGFR2 or VEGFR2 in HepG2 cells. A significant decrease in the levels of pSTAT3 was only detected in case of sorafenib-ramucirumab combination. The combined treatment of sorafenib with panitumumab induced a significant arrest in pre-G and G2/M cell cycle phases and significantly decreased the relative expression of EGFR and MMP-9. Sorafenib-ramucirumab combination showed enhanced apoptosis, inhibited proliferation and angiogenesis in HepG2 cancer cells. Our findings suggest that ramucirumab can be a useful as an adjunct therapy for improvement of sorafenib efficacy in suppression of HCC.

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Section: Introductionmentioning

confidence: 99%

Ramucirumab combination with sorafenib enhances the inhibitory effect of sorafenib on HepG2 cancer cells

Taha

Aboulwafa

Zedan

et al. 2022

Sci Rep

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“…Angiogenesis in our wet AMD BOECs was driven by interleukin signaling and amino acid metabolism. While these processes have not been well reported in the pathogenesis of CNV, our wet AMD BOECs reflected pathological angiogenesis mechanisms observed in other diseases with vasculopathy or aberrant vessel growth, such as in tumor angiogenesis [ 89 , 90 , 91 ]. On the other hand, the normal control BOECs featured physiological angiogenesis mediated by VEGF, PDGF and Eph-Ephrin signaling.…”

Section: Discussionmentioning

confidence: 50%

Single-Cell Transcriptome of Wet AMD Patient-Derived Endothelial Cells in Angiogenic Sprouting

Yeo

Wazny

Nguyen

et al. 2022

IJMS

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Age-related macular degeneration (AMD) is a global leading cause of visual impairment in older populations. ‘Wet’ AMD, the most common subtype of this disease, occurs when pathological angiogenesis infiltrates the subretinal space (choroidal neovascularization), causing hemorrhage and retinal damage. Gold standard anti-vascular endothelial growth factor (VEGF) treatment is an effective therapy, but the long-term prevention of visual decline has not been as successful. This warrants the need to elucidate potential VEGF-independent pathways. We generated blood out-growth endothelial cells (BOECs) from wet AMD and normal control subjects, then induced angiogenic sprouting of BOECs using a fibrin gel bead assay. To deconvolute endothelial heterogeneity, we performed single-cell transcriptomic analysis on the sprouting BOECs, revealing a spectrum of cell states. Our wet AMD BOECs share common pathways with choroidal neovascularization such as extracellular matrix remodeling that promoted proangiogenic phenotype, and our ‘activated’ BOEC subpopulation demonstrated proinflammatory hallmarks, resembling the tip-like cells in vivo. We uncovered new molecular insights that pathological angiogenesis in wet AMD BOECs could also be driven by interleukin signaling and amino acid metabolism. A web-based visualization of the sprouting BOEC single-cell transcriptome has been created to facilitate further discovery research.

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“…Tumor angiogenesis plays a vital role in tumorigenesis and development. Angiogenesis refers to developing new blood vessels from existing capillaries or postcapillary veins [ 119 , 120 ]. Generally, the whole process of angiogenesis occured in tissues is coordinated by angiogenic and vasopressor factors [ 121 , 122 ].…”

Section: The Roles Of Texs In Angiogenesismentioning

confidence: 99%

Tumor-derived small extracellular vesicles: potential roles and mechanism in glioma

2022

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Small extracellular vesicles (SEVs) are extracellular vesicles containing DNA, RNA, and proteins and are involved in intercellular communication and function, playing an essential role in the growth and metastasis of tumors. SEVs are present in various body fluids and can be isolated and extracted from blood, urine, and cerebrospinal fluid. Under both physiological and pathological conditions, SEVs can be released by some cells, such as immune, stem, and tumor cells, in a cytosolic manner. SEVs secreted by tumor cells are called tumor-derived exosomes (TEXs) because of their origin in the corresponding parent cells. Glioma is the most common intracranial tumor, accounting for approximately half of the primary intracranial tumors, and is characterized by insidious onset, high morbidity, and high mortality rate. Complete removal of tumor tissues by surgery is difficult. Chemotherapy can improve the survival quality of patients to a certain extent; however, gliomas are prone to chemoresistance, which seriously affects the prognosis of patients. In recent years, TEXs have played a vital role in the occurrence, development, associated immune response, chemotherapy resistance, radiation therapy resistance, and metastasis of glioma. This article reviews the role of TEXs in glioma progression, drug resistance, and clinical diagnosis.

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Role of Cytokines and Chemokines in Angiogenesis in a Tumor Context

Cited by 58 publications

References 161 publications

Ramucirumab combination with sorafenib enhances the inhibitory effect of sorafenib on HepG2 cancer cells

Ramucirumab combination with sorafenib enhances the inhibitory effect of sorafenib on HepG2 cancer cells

Single-Cell Transcriptome of Wet AMD Patient-Derived Endothelial Cells in Angiogenic Sprouting

Tumor-derived small extracellular vesicles: potential roles and mechanism in glioma

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