Vascular endothelial growth factors synthesized by human lung mast cells exert angiogenic effects

Detoraki, Aikaterini; Staiano, Rosaria Ilaria; Granata, Francescopaolo; Giannattasio, Giorgio; Prevete, Nella; Paulis, Amato de; Ribatti, Doménico; Genovese, Arturo; Triggiani, Massimo; Marone, Gianni

doi:10.1016/j.jaci.2009.01.044

Cited by 187 publications

(220 citation statements)

References 38 publications

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“…TC cells, TAMs, TAMCs and other immune cells are a major source of proangiogenic and lymphangiogenic molecules. 53,54 Interestingly, immune cells and tumors can produce pro-and anti-angiogenic isoforms of VEGFs. 62 A deeper knowledge of the balance between these isoforms could lead to the discovery of novel targets that can be manipulated to block TC growth.…”

Section: Discussionmentioning

confidence: 99%

“…TC cells and immune cells are a major source of several protumorigenic and proangiogenic cytokines/chemokines. 53 Targeting these mediators could be exploited to block TC growth, since this strategy has been already developed for other tumors. 116 Moreover, boosting anticancer immune responses by blocking immunosuppressive molecules (TGF-b, IL-10, CTLA-4, PD-1 and PD-L1) expressed either by cancer cells or by tumor-infiltrating immune cells 117 and cytolytic viruses approaches 51 appear promising therapeutic strategies in different tumors, including TC.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, MCs are a major source of proangiogenic (VEGF-A and -B) and lymphangiogenic (VEGF-C and -D) factors. 53 In addition, thyroid MCs modulated angiogenesis through the release of CXCL8/IL-8. 25 Human macrophages are also a major source of both angiogenic and lymphangiogenic factors 54 as well as of several proangiogenic enzymes such as MMP-9, Cox-2 and iNOS.…”

Section: Angiogenic Factorsmentioning

confidence: 99%

“…79 TC cell line CM induced in vitro MC chemotaxis through the release of VEGF-A, 24 which activated the VEGFRs on human MCs. 53,80 In addition, TC cells activated MCs to release cytokines (IL-6, TNF-a, GM-CSF) and chemokines (CXCL10/ IP10 and CXCL1/Gro-a). In turn, MCs promoted TC cell proliferation through CXCL1/GROa and CXCL10/IP10.…”

Section: Dendritic Cells (Dcs)mentioning

confidence: 99%

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The immune network in thyroid cancer

2016

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The immune system plays critical roles in tumor prevention, but also in its initiation and progression. Tumors are subjected to immunosurveillance, but cancer cells generate an immunosuppressive microenvironment that favors their escape from immune-mediated elimination. During chronic inflammation, immune cells can contribute to the formation and progression of tumors by producing mitogenic, prosurvival, proangiogenic and lymphangiogenic factors. Thyroid cancer is the most frequent type of endocrine neoplasia and is the most rapidly increasing cancer in the US. In this review, we discuss recent findings on how different immune cells and mediators can contribute to thyroid cancer development and progression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Angiogenic Factorsmentioning

confidence: 99%

Section: Dendritic Cells (Dcs)mentioning

confidence: 99%

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The immune network in thyroid cancer

2016

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“…In several human tumors, including thyroid cancer and related animal models, it has been observed that tumor angiogenesis correlates with the extent of macrophage infiltration (Russell et al, 2003;Detoraki et al, 2009). To investigate the presence of infiltrating macrophages in our in vivo tumor model, we evaluated their presence at tumor edges by immunohistochemistry with F4/80 antibodies.…”

Section: Effect Of Timp3 Restoration In Mouse Tumor Xenograftsmentioning

confidence: 99%

TIMP3 regulates migration, invasion and in vivo tumorigenicity of thyroid tumor cells

et al. 2011

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Papillary thyroid carcinoma (PTC) arises from the thyroid follicular epithelium and represents the most frequent thyroid malignancy. PTC is associated with gene rearrangements generating RET/PTC and TRK oncogenes, and to the BRAFV600E activating point mutation. A role of tumor-suppressor genes in the pathogenesis of PTC has not been assessed yet. The tissue inhibitor of metalloproteinase-3 (TIMP3) gene, encoding a metalloproteinases inhibitor and capable of inhibiting growth, angiogenesis, invasion and metastasis of several cancers, was found to be silenced by promoter methylation in a consistent fraction of PTCs, in association with tumor aggressiveness and BRAFV600E mutation, thus suggesting an oncosuppressor role. To explore this possibility, in this study we performed gene expression and functional studies. Analysis of gene expression data produced in our laboratory as well as meta-analysis of publicly available data sets confirmed the downregulation of TIMP3 gene expression in PTC with respect to normal thyroid. The functional consequences of TIMP3 downregulation were investigated in the PTC-derived NIM1 cell line, in which the expression of TIMP3 is silenced. Restoration of TIMP3 expression by exposure to soluble TIMP3 protein or by complementary DNA transfection had no effect on the growth rate of NIM1 cells. Instead, it affected the adhesive, migratory and invasive capabilities of NIM1 cells by modulating several proteins involved in these processes. A striking effect was observed in vivo, as TIMP3 reduced the tumorigenicity of NIM1 cells by repressing angiogenesis and macrophage infiltration. Our data indicate that the loss of TIMP3 expression exerts a functional role in the pathogenesis of PTC.

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Mast cell‐based molecular subtypes and signature associated with clinical outcome in early‐stage lung adenocarcinoma

et al. 2020

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Mast cells are a major component of the immune microenvironment in tumour tissues and modulate tumour progression by releasing pro-tumorigenic and antitumorigenic molecules. Regarding the impact of mast cells on the outcomes of patients with lung adenocarcinoma (LUAD) patient, several published studies have shown contradictory results. Here, we aimed at elucidating the role of mast cells in early-stage LUAD. We found that high mast cell abundance was correlated with prolonged survival in earlystage LUAD patients. The mast cell-related gene signature and gene mutation data sets were used to stratify early-stage LUAD patients into two molecular subtypes (subtype 1 and subtype 2). The neural network-based framework constructed with the mast cell-related signature showed high accuracy in predicting response to immunotherapy. Importantly, the prognostic mast cell-related signature predicted the survival probability and the potential relationship between TP53 mutation, c-MYC activation and mast cell activities. The meta-analysis confirmed the prognostic value of the mast cell-related gene signature. In summary, this study might improve our understanding of the role of mast cells in early-stage LUAD and aid in the development of immunotherapy and personalized treatments for early-stage LUAD patients.

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Vascular endothelial growth factors synthesized by human lung mast cells exert angiogenic effects

Cited by 187 publications

References 38 publications

The immune network in thyroid cancer

The immune network in thyroid cancer

TIMP3 regulates migration, invasion and in vivo tumorigenicity of thyroid tumor cells

Mast cell‐based molecular subtypes and signature associated with clinical outcome in early‐stage lung adenocarcinoma

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