Support of Tumor Endothelial Cells by Chemokine Receptors

Salazar, Nicole; Zabel, Brian A.

doi:10.3389/fimmu.2019.00147

Cited by 56 publications

(33 citation statements)

References 91 publications

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“…In most solid tumors, endothelial cells (ECs) build up the inner layer of the blood vessels as part of a growing tumor [40]. Compared to normal ECs, tumor-derived endothelial cells (TECs) have a disturbed morphology and phenotypes at the cellular and molecular levels, similar to the tumor itself [40][41][42]. Considering their origin, tumor-derived endothelial cells (TECs) can be produced directly by differentiation of cancer cells, where they allow ECs to migrate into the tumor or eventually leave the tumor.…”

Section: Tumor Endothelial Cells (Tecs)mentioning

confidence: 99%

“…Tumor hypoxia induces angiogenesis by activating the expression of vascular endothelial growth factor (VEGF) [3]. Meanwhile, TECs use various chemokine receptors (CXCR) including atypical chemokine receptor 1 (ACKR1), ACKR3, CXCR7, CXCR4, and chemokine (C-C motif) receptor 2 (CCR2) as markers of TECs to support tumor cells progression in numerous cancer types, recently reviewed in [40]).…”

Section: Tumor Endothelial Cells (Tecs)mentioning

confidence: 99%

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Tumor microenvironment complexity and therapeutic implications at a glance

et al. 2020

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The dynamic interactions of cancer cells with their microenvironment consisting of stromal cells (cellular part) and extracellular matrix (ECM) components (non-cellular) is essential to stimulate the heterogeneity of cancer cell, clonal evolution and to increase the multidrug resistance ending in cancer cell progression and metastasis. The reciprocal cell-cell/ECM interaction and tumor cell hijacking of non-malignant cells force stromal cells to lose their function and acquire new phenotypes that promote development and invasion of tumor cells. Understanding the underlying cellular and molecular mechanisms governing these interactions can be used as a novel strategy to indirectly disrupt cancer cell interplay and contribute to the development of efficient and safe therapeutic strategies to fight cancer. Furthermore, the tumor-derived circulating materials can also be used as cancer diagnostic tools to precisely predict and monitor the outcome of therapy. This review evaluates such potentials in various advanced cancer models, with a focus on 3D systems as well as lab-on-chip devices.

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Section: Tumor Endothelial Cells (Tecs)mentioning

confidence: 99%

Section: Tumor Endothelial Cells (Tecs)mentioning

confidence: 99%

Tumor microenvironment complexity and therapeutic implications at a glance

et al. 2020

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“…The activity of CXCR4 is mainly γ-mediated; however, CXCR7 is considered to be an atypical G protein-coupled receptor, as it does not cause intracellular Ca 2+ release when bound to a ligand ( 107 ). Some studies have shown that CXCR7 is a DcR that isolates extracellular CXCL12 or regulates the CXCR4 signaling pathway by forming a CXCR7-CXCR4 heterodimer ( 108 , 109 ). High expression of CXCR7 in human cancer types such as bladder cancer, glioma, colorectal cancer, ovarian cancer and breast cancer, and in tumor-associated blood vessels, may be critical for tumor cell survival, adhesion and growth ( 110 – 115 ).…”

Section: Role Of Inflammation Factors and Immune-related Cells In Thementioning

confidence: 99%

Impact of inflammation and immunotherapy in renal cell carcinoma (Review)

et al. 2020

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Substantial research attention has been directed at exploring the mechanisms and treatment of renal cell carcinoma (RCC). Indeed, the association between inflammation and tumor phenotypes has been at the center of cancer research. Concomitant with research on the inflammation response and inflammatory molecules involved in RCC, new breakthroughs have emerged. A large body of knowledge now shows that treatments targeting inflammation and immunity in RCC provide substantial clinical benefits. Adequate analysis and a better understanding of the mechanisms of inflammatory factors in the occurrence and progression of RCC are highly desirable. Currently, numerous RCC treatments targeted at inflammation and immunotherapy are available. The current review describes in detail the link between inflammation and RCC.

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“…In contrast to melanoma, anti-CXCR2 therapy did not reduce tumor weight in the mesothelioma mouse model ( Figure S7 ). Since CXCR2 may also stimulate tumor endothelial cells [ 34 ], we measured the expression of intratumoral CD31 and found no changes upon the therapy ( Figure S8 ), indicating the absence of effect on tumor vascularization.…”

Section: Resultsmentioning

confidence: 99%

Blocking Migration of Polymorphonuclear Myeloid-Derived Suppressor Cells Inhibits Mouse Melanoma Progression

Groth

Arpinati

Shaul

et al. 2021

Cancers

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Background: Despite recent improvement in the treatment of malignant melanoma by immune-checkpoint inhibitors, the disease can progress due to an immunosuppressive tumor microenvironment (TME) mainly represented by myeloid-derived suppressor cells (MDSC). However, the relative contribution of the polymorphonuclear (PMN) and monocytic (M) MDSC subsets to melanoma progression is not clear. Here, we compared both subsets regarding their immunosuppressive capacity and recruitment mechanisms. Furthermore, we inhibited PMN-MDSC migration in vivo to determine its effect on tumor progression. Methods: Using the RET transgenic melanoma mouse model, we investigated the immunosuppressive function of MDSC subsets and chemokine receptor expression on these cells. The effect of CXCR2 inhibition on PMN-MDSC migration and tumor progression was studied in RET transgenic mice and in C57BL/6 mice after surgical resection of primary melanomas. Results: Immunosuppressive capacity of intratumoral M- and PMN-MDSC was comparable in melanoma bearing mice. Anti-CXCR2 therapy prolonged survival of these mice and decreased the occurrence of distant metastasis. Furthermore, this therapy reduced the infiltration of melanoma lesions and pre-metastatic sites with PMN-MDSC that was associated with the accumulation of natural killer (NK) cells. Conclusions: We provide evidence for the tumor−promoting properties of PMN-MDSC as well as for the anti-tumor effects upon their targeting in melanoma bearing mice.

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Support of Tumor Endothelial Cells by Chemokine Receptors

Cited by 56 publications

References 91 publications

Tumor microenvironment complexity and therapeutic implications at a glance

Tumor microenvironment complexity and therapeutic implications at a glance

Impact of inflammation and immunotherapy in renal cell carcinoma (Review)

Blocking Migration of Polymorphonuclear Myeloid-Derived Suppressor Cells Inhibits Mouse Melanoma Progression

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