Inflammatory cytokines prime adipose tissue mesenchymal stem cells to enhance malignancy of <scp>MCF</scp>‐7 breast cancer cells via transforming growth factor‐β1

Trivanović, Drenka; Jauković, Aleksandra; Krstić, Jelena; Nikolić, Srdjan; Djordjević, Ivana; Кукољ, Тамара; Obradović, Hristina; Mojsilović, Slavko; Ilić, Vesna; Santibáñez, Juan F.; Bugarski, Diana

doi:10.1002/iub.1473

Cited by 42 publications

(36 citation statements)

References 50 publications

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“…Expression of TGF- β in adipose tissue MSCs can be stimulated by inflammatory cytokines presented in TME, such as IFN- γ and TNF- α . It has been reported that TGF- β produced by cytokine-primed adipose tissue MSCs contribute to EMT, migration, and invasiveness of breast cancer cells [103]. These findings indicate important role of TGF- β not only in regulation of tumor cells behavior, but also in determination of MSC activity in inflammatory TME.…”

Section: Tgf-βmentioning

confidence: 73%

The Roles of Mesenchymal Stromal/Stem Cells in Tumor Microenvironment Associated with Inflammation

Trivanović

Krstić

Djordjević

et al. 2016

Mediators of Inflammation

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State of tumor microenvironment (TME) is closely linked to regulation of tumor growth and progression affecting the final outcome, refractoriness, and relapse of disease. Interactions of tumor, immune, and mesenchymal stromal/stem cells (MSCs) have been recognized as crucial for understanding tumorigenesis. Due to their outstanding features, stem cell-like properties, capacity to regulate immune response, and dynamic functional phenotype dependent on microenvironmental stimuli, MSCs have been perceived as important players in TME. Signals provided by tumor-associated chronic inflammation educate MSCs to alter their phenotype and immunomodulatory potential in favor of tumor-biased state of MSCs. Adjustment of phenotype to TME and acquisition of tumor-promoting ability by MSCs help tumor cells in maintenance of permissive TME and suppression of antitumor immune response. Potential utilization of MSCs in treatment of tumor is based on their inherent ability to home tumor tissue that makes them suitable delivery vehicles for immune-stimulating factors and vectors for targeted antitumor therapy. Here, we review data regarding intrusive effects of inflammatory TME on MSCs capacity to affect tumor development through modification of their phenotype and interactions with immune system.

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Section: Tgf-βmentioning

confidence: 73%

The Roles of Mesenchymal Stromal/Stem Cells in Tumor Microenvironment Associated with Inflammation

Trivanović

Krstić

Djordjević

et al. 2016

Mediators of Inflammation

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“…MSCs are able to effectively inhibit the proliferation of T-cells, B-cells, NK, and dendritic cells because of their production and secretion of molecules such as TGF- β , PGE2, and indoleamine-pyrrole 2,3-dioxygenase (IDO) [171, 172]. Furthermore, Tumor Necrosis Factor Alfa (TNF- α ) activates MSCs to secrete chemokine (C-C motif) ligand 5 (CCL5), C-C chemokine receptor type 2 (CCR2), and the interleukin 8 receptor, beta ( CXCR2) ligands that in turn recruit CXCR2+ neutrophils into the tumor.…”

Section: Mscs and Cancer Cellsmentioning

confidence: 99%

Stemness in Cancer: Stem Cells, Cancer Stem Cells, and Their Microenvironment

Aponte

Caicedo²

2017

Stem Cells International

308

187

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Stemness combines the ability of a cell to perpetuate its lineage, to give rise to differentiated cells, and to interact with its environment to maintain a balance between quiescence, proliferation, and regeneration. While adult Stem Cells display these properties when participating in tissue homeostasis, Cancer Stem Cells (CSCs) behave as their malignant equivalents. CSCs display stemness in various circumstances, including the sustaining of cancer progression, and the interaction with their environment in search for key survival factors. As a result, CSCs can recurrently persist after therapy. In order to understand how the concept of stemness applies to cancer, this review will explore properties shared between normal and malignant Stem Cells. First, we provide an overview of properties of normal adult Stem Cells. We thereafter elaborate on how these features operate in CSCs. We then review the organization of microenvironment components, which enables CSCs hosting. We subsequently discuss Mesenchymal Stem/Stromal Cells (MSCs), which, although their stemness properties are limited, represent essential components of the Stem Cell niche and tumor microenvironment. We next provide insights of the therapeutic strategies targeting Stem Cell properties in tumors and the use of state-of-the-art techniques in future research. Increasing our knowledge of the CSCs microenvironment is key to identifying new therapeutic solutions.

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“…TNFα is present in high concentrations throughout the breast tumor/ stroma milieu, and upon activation of TNFα receptors, can trigger a powerful perpetual cascade of NF-κB activation [23,24]. epithelial-to-mesenchymal transition [25] and sustained release of diverse chemokines (i.e., CCL2/CCL5) [26]. Chemokines in turn ultimately trigger inward migration of a large number of leukocyte sub-populations (LSPs) bearing CCR2 / CCR5 receptors that embed into the tumor, and further drive tumor aggression and stem cell survival.…”

Section: Introductionmentioning

confidence: 99%

Apigenin inhibits TNFα/IL-1α-induced CCL2 release through IKBK-epsilon signaling in MDA-MB-231 human breast cancer cells

et al. 2017

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Mortality associated with breast cancer is attributable to aggressive metastasis, to which TNFα plays a central orchestrating role. TNFα acts on breast tumor TNF receptors evoking the release of chemotactic proteins (e.g. MCP-1/CCL2). These proteins direct inward infiltration/migration of tumor-associated macrophages (TAMs), tumor-associated neutrophils (TANs), myeloid-derived suppressor cells (MDSCs), T-regulatory cells (Tregs), T helper IL-17-producing cells (Th17s), metastasis-associated macrophages (MAMs) and cancer-associated fibroblasts (CAFs). Tumor embedded infiltrates collectively enable immune evasion, tumor growth, angiogenesis, and metastasis. In the current study, we investigate the potential of apigenin, a known anti-inflammatory constituent of parsley, to downregulate TNFα mediated release of chemokines from human triple-negative cells (MDA-MB-231 cells). The results show that TNFα stimulation leads to large rise of CCL2, granulocyte macrophage colony-stimulating factor (GMCSF), IL-1α and IL-6, all suppressed by apigenin. While many aspects of the transcriptome for NFkB signaling were evaluated, the data show signaling patterns associated with CCL2 were blocked by apigenin and mediated through suppressed mRNA and protein synthesis of IKBKe. Moreover, the data show that the attenuation of CCL2 by apigenin in the presence TNFα paralleled the suppression of phosphorylated extracellular signal-regulated kinase 1 (ERK 1/ 2). In summary, the obtained findings suggest that there exists a TNFα evoked release of CCL2 and other LSP recruiting cytokines from human breast cancer cells, which can be attenuated by apigenin.

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Inflammatory cytokines prime adipose tissue mesenchymal stem cells to enhance malignancy of MCF‐7 breast cancer cells via transforming growth factor‐β1

Cited by 42 publications

References 50 publications

The Roles of Mesenchymal Stromal/Stem Cells in Tumor Microenvironment Associated with Inflammation

The Roles of Mesenchymal Stromal/Stem Cells in Tumor Microenvironment Associated with Inflammation

Stemness in Cancer: Stem Cells, Cancer Stem Cells, and Their Microenvironment

Apigenin inhibits TNFα/IL-1α-induced CCL2 release through IKBK-epsilon signaling in MDA-MB-231 human breast cancer cells

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