Correction: Differential Contribution of Acute and Chronic Inflammation to the Development of Murine Mammary 4T1 Tumors

Viana, Celso Tarso Rodrigues; Castro, Pollyana Ribeiro; Marques, Suzane M.; Lopes, Míriam Teresa Paz; Gonçalves, Ricardo; Campos, Paula Peixoto; Andrade, Sílvia Passos

doi:10.1371/journal.pone.0138408

Cited by 4 publications

(4 citation statements)

References 1 publication

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“…In a previously published study, mice were inoculated with 4T1 cells and implanted with sponge discs for 1 or 24 days to create acute and chronic inflammatory environments [ 25 ]. Tumor progression and circulating levels of VEGF and TNF- α were greater in the presence of chronic inflammation than acute inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…Tumor progression and circulating levels of VEGF and TNF- α were greater in the presence of chronic inflammation than acute inflammation. In addition, VEGF and TNF- α molecules are critical for the proliferation, angiogenesis, macrophage recruitment, and metastasis associated with tumor progression [ 25 ]. Populations of macrophages, dendritic cells, and lymphocytes were significantly larger in mice with chronic inflammation [ 25 ], suggesting that chronic cell infiltration is important for tumor progression.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, VEGF and TNF- α molecules are critical for the proliferation, angiogenesis, macrophage recruitment, and metastasis associated with tumor progression [ 25 ]. Populations of macrophages, dendritic cells, and lymphocytes were significantly larger in mice with chronic inflammation [ 25 ], suggesting that chronic cell infiltration is important for tumor progression. In an obesity-related breast cancer study, 4Tl cell proliferation was significantly observed when cells were cultured in adipocyte-conditioned medium without any stimulation, indicating that spontaneous adipocyte infiltration contributed to 4T1 cell growth [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

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Aspirin Disrupts the Crosstalk of Angiogenic and Inflammatory Cytokines between 4T1 Breast Cancer Cells and Macrophages

Hsieh

Wang

2018

Mediators of Inflammation

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The tumor microenvironment is rich in multiple cell types that influence tumor development. Macrophages infiltrate tumors, where they are the most abundant immune cell population and secrete a number of cytokines. Aspirin acts as a chemopreventive agent against cancer development. This study investigated whether aspirin regulates crosstalk between breast cancer cells and macrophages. To study these interactions in a tumor microenvironment, a conditioned media was employed using 4T1 breast cancer cells cultured in RAW 264.7 cell-conditioned medium (RAW-CM), and a cocultured model of both cells was used. When 4T1 cells were cultured in the RAW-CM, there were increases in cell viability and secretion of the cytokines VEGF, PAI-1, TNF-α, and IL-6. Treatment with aspirin inhibited 4T1 cell growth and migration and MCP-1, PAI-1, and IL-6 production. In the coculture of both cells, aspirin inhibited secretion of MCP-1, IL-6, and TGF-β. Furthermore, aspirin significantly decreased the M2 macrophage marker CD206, but increased M1 marker CD11c expression. In summary, aspirin treatment inhibited the crosstalk of 4T1 and RAW 264.7 cells through regulation of angiogenic and inflammatory mediator production and influenced the M1/M2 macrophage subtype. This highlighted that aspirin suppresses the tumor favorable microenvironment and could be a promising agent against triple-negative breast cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Aspirin Disrupts the Crosstalk of Angiogenic and Inflammatory Cytokines between 4T1 Breast Cancer Cells and Macrophages

Hsieh

Wang

2018

Mediators of Inflammation

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“…It has been demonstrated that the level of VEGF is elevated in the circulation of obese people, and is accompanied by tumor expression, which is associated with a poor prognosis in obesity-related cancers [ 12 , 33 ]. Recently, it was revealed that the levels of VEGF and TNF-α in serum of tumor bearing mice were higher than the control group after implanting 4T1 cells for 10 days, but the CCL2 level was increased quickly after implantation [ 34 ]. It is clear that these inflammatory mediators are a response to breast tumor growth.…”

Section: Discussionmentioning

confidence: 99%

Aspirin Breaks the Crosstalk between 3T3-L1 Adipocytes and 4T1 Breast Cancer Cells by Regulating Cytokine Production

Hsieh

Huang

2016

PLoS ONE

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Breast cancer is one of the most common cancers in women worldwide. The obesity process is normally accompanied by chronic, low-grade inflammation. Infiltration by inflammatory cytokines and immune cells provides a favorable microenvironment for tumor growth, migration, and metastasis. Epidemiological evidence has shown that aspirin is an effective agent against several types of cancer. The aim of this study is to investigate the anti-inflammatory and anti-cancer effects of aspirin on 3T3-L1 adipocytes, 4T1 murine breast cancer cells, and their crosstalk. The results showed that aspirin treatment inhibited differentiation and lipid accumulation by 3T3-L1 preadipocytes, and decreased the secretion of the inflammatory adipokine MCP-1 after stimulation with tumor necrosis factor (TNF)-α or conditioned medium from RAW264.7 cells. In 4T1 cells, treatment with aspirin decreased cell viability and migration, possibly by suppressing MCP-1 and VEGF secretion. Subsequently, culture of 4T1 cells in 3T3-L1 adipocyte-conditioned medium (Ad-CM) and co-culture of 3T3-L1 and 4T1 cells using a transwell plate were performed to clarify the relationship between these two cell lines. Aspirin exerted its inhibitory effects in the transwell co-culture system, as well as the conditioned-medium model. Aspirin treatment significantly inhibited the proliferation of 4T1 cells, and decreased the production of MCP-1 and PAI-1 in both the Ad-CM model and co-culture system. Aspirin inhibited inflammatory MCP-1 adipokine production by 3T3-L1 adipocytes and the cell growth and migration of 4T1 cells. It also broke the crosstalk between these two cell lines, possibly contributing to its chemopreventive properties in breast cancer. This is the first report that aspirin’s chemopreventive activity supports the potential application in auxiliary therapy against obesity-related breast cancer development.

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Cytokine Production Is Differentially Modulated in Malignant and Non-malignant Tissues in ST2-Receptor Deficient Mice

et al. 2018

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IL-33/ST2 axis has been shown to exert both pro- and anti- effects in wound healing and tumor development. To further understand the role of this cytokine complex, we characterized comparatively the inflammatory component of a malignant tissue and non-malignant tissue in mice lacking ST2 receptor (ST2-KO). KO mice and their wild-type (WT) counterparts were either implanted subcutaneously with polyether-polyurethane sponge discs to induce non-malignant fibrovascular tissue growth or inoculated with 4T1 cells to induce mammary tumor. Loss of ST2 receptor in mice resulted in enhanced mammary tumor and fibrovascular tissue relative to the WT animals. The inflammatory parameters (MPO and NAG activities, levels of the cytokines CXCL1/KC, CCL2, TNF-α, TGF-β1, and mast cell number) were differentially modulated in both tissues. In tumors, these parameters were, overall, lower compared with those in tumors of WT mice. In KO implants, CXCL1/KC and TNF-α levels increased; MPO, NAG, and CCL2 levels decreased relative to the WT implants. In addition, deletion of ST2 receptor inhibited mast cell recruitment but had no effect on TGF-β1 levels in implants. Our study has shown antitumorigenic effect of ST2 in mammary tumor and this may be mediated by downregulation of pro-inflammatory cytokines (CXCL1/KC, CCL2, TNF-α, and TGF-β1). Conversely, in the fibrovascular tissue, lack of ST2 receptor resulted in differential modulation of cytokine production. Differential signaling mechanisms may be activated by IL-33/ST2 axis to modulate cytokine production in malignant and non-malignant proliferative processes.

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Correction: Differential Contribution of Acute and Chronic Inflammation to the Development of Murine Mammary 4T1 Tumors

Cited by 4 publications

References 1 publication

Aspirin Disrupts the Crosstalk of Angiogenic and Inflammatory Cytokines between 4T1 Breast Cancer Cells and Macrophages

Aspirin Disrupts the Crosstalk of Angiogenic and Inflammatory Cytokines between 4T1 Breast Cancer Cells and Macrophages

Aspirin Breaks the Crosstalk between 3T3-L1 Adipocytes and 4T1 Breast Cancer Cells by Regulating Cytokine Production

Cytokine Production Is Differentially Modulated in Malignant and Non-malignant Tissues in ST2-Receptor Deficient Mice

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