CCL2-induced chemokine cascade promotes breast cancer metastasis by enhancing retention of metastasis-associated macrophages

Kitamura, Takanori; Qian, Bin‐Zhi; Soong, Daniel; Cassetta, Luca; Noy, Roy; Sugano, Gaël; Kato, Yu; Li, Jiufeng; Pollard, Jeffrey W.

doi:10.1084/jem.20141836

Cited by 536 publications

(416 citation statements)

References 58 publications

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“…This is consistent with other studies showing that intravenously injected B16 melanoma cells develop more lung metastatic foci in Ccl3 -/ -mice than WT mice [10]. However, recent studies demonstrated that IMo are retained in the metastatic site through a CCL3-dependent mechanism [11] and promote tumor cell survival. It would be interesting to assess using conditional genetics whether PMo-derived CCL3 recruits NK cells and at the same time affects MAM retention.…”

supporting

confidence: 93%

Cancer immunosurveillance: role of patrolling monocytes

Cassetta

Pollard

2015

Cell Res

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npg Classical inflammatory monocytes and their derivative macrophages promote tumor metastasis whereas CD8 + T and NK cells restrict tumor growth. In a recent paper published in Science, Hanna and colleagues demonstrate that another monocyte population, nonclassical patrolling monocytes, is enriched in the microvasculature of tumor-challenged lung and reduces tumor metastasis by recruiting NK cells.Tumor metastasis accounts for 95% of cancer-related deaths in the developed world. In the past decade focus has shifted from study of cancer cells alone to the tumor microenvironment that consists of many cell types that overall support cancer progression. Circulating monocytes extravasate into the tissue and differentiate into macrophages, which are key players in the regulation of metastasis as they provide support for the extravasation, survival and growth of metastatic cancer cells [1].There are at least two circulating monocyte populations in the blood: classical "inflammatory" monocytes (IMo, CCR2 High Ly6C + in mouse; CCR2 High CD14 ++ CD16 -in human) and nonclassical "patrolling" monocytes (PMo, CX3CR1 High Ly6C -in mouse; CX3CR1 High CD14 + CD16 + in human). IMo are recruited to inflammatory sites through the CCR2-CCL2 axis; they extravasate, differentiate into tissue macrophages and dendritic cells, and respond to bacterial and parasitic infections. In breast cancer models, IMo are also recruited via the CCL2-CCR2 axis to metastatic sites where they promote cancer cell extravasation and survival [2].

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supporting

confidence: 93%

Cancer immunosurveillance: role of patrolling monocytes

Cassetta

Pollard

2015

Cell Res

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“…30,31 CCL-2 and CCL-3 in lung metastasis have not been fully discussed. However, a recent study which was conducted by Kitamura et al 32 demonstrated that CCL-2 had a therapeutic impact in breast cancer metastasis through enhancing several macrophages retention. Meanwhile, abundant evidence have referred the pivotal carcinogenesis of IL-8 in lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Benzopyrene promotes lung cancer A549 cell migration and invasion through up-regulating cytokine IL8 and chemokines CCL2 and CCL3 expression

Zhang

Jin

et al. 2016

Exp Biol Med (Maywood)

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Tobacco-sourced carcinogen including benzopyrene (B[a]P) in lung cancer metastasis has not been fully reported. In this study, lung carcinoma A549 cell line was used to investigate the potential roles of tobacco-sourced B[a]P on cell metastasis and invasion and to assess its underlying mechanism. Effects of tobacco-sourced carcinogen on A549 cell proliferation, metastasis, and invasion were analyzed using MTT assay, Transwell assay, and scratch method, respectively. The effects of tobacco-sourced carcinogen on cytokines and chemokines secretion were detected using enzyme-linked immunosorbent assay. Moreover, correlation between inflammatory factor expression and cancer cell migration and invasion was assessed using siRNA-mediated gene silencing. Data showed that both B[a]P and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone either at high or low dose performed no significant difference on A549 cell proliferation with time increasing. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone performed no significant difference on A549 cell migration and invasion while B[a]P significantly increased A549 cell migration and invasion compared to the control group (P < 0.05). Consequently, except for IL-6, IL-8, CCL-2, and CCL-3, secretions were significantly increased by B[a]P treatment compared to the control (P < 0.05). Furthermore, when CCL-2 and CCL-3 were silenced, the migrated and invasive A549 cells were significantly decreased compared to the control, respectively (P < 0.05), while silenced IL-8 drastically decreased the migrated and invasive cells compared to the control (P < 0.01). Taken together, this study illustrated that there may be significant correlation between smoking and lung cancer metastasis. B[a]P maybe an excellent contributor for lung cancer metastasis through up-regulating IL-8, CCL-2, and CCL-3 expression.

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“…The multiple studies have illustrated that CCL2/CCR2 axis signaling-mediated crosstalk between TAMs and tumor cells plays a critical role in macrophage recruitment in hepatocellular carcinoma and prostate cancer. [31][32][33] In light of this, we conducted western blotting and RT-qPCR assay to analyze the levels of key cytokines CCL2 secreted into medium. As expected, PKM2-shRNA treatment or siRNA-PKM2 transfection into HT-29 and Caco-2 cells caused a significant reduction in expression of mRNA and protein levels in CCL2 (Figure 3(a) and (b)).…”

Section: Pkm2 Contributes To Macrophage Recruitment By Regulation Ofmentioning

confidence: 99%

Specific tumor-derived CCL2 mediated by pyruvate kinase M2 in colorectal cancer cells contributes to macrophage recruitment in tumor microenvironment

Zou

Wang

et al. 2017

Tumour Biol.

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Development of colorectal cancer has been considered as a result of imbalance of pro-and anti-inflammatory intestinal microenvironment accompanied by macrophage recruitment. Despite macrophages are implicated in remodeling tumor microenvironment, the mechanism of macrophage recruitment is not fully elucidated yet. In this study, we reported clinical association of highly expressed pyruvate kinase M2 in colorectal cancer with macrophage attraction. The conditioned medium from Caco-2 and HT-29 cells with depleted pyruvate kinase M2 dramatically reduced macrophage recruitment, which is reversed by addition of, a critical chemotaxis factor to macrophage migration, rCCL2. Silencing of endogenous pyruvate kinase M2 markedly decreased CCL2 expression and secretion by real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay. Endogenous pyruvate kinase M2 interacted with p65 and mediated nuclear factor-κB signaling pathway and mainly regulated phosphorylation of Ser276 on p65 nuclear factor-κB. In addition, inhibition of macrophage recruitment caused by pyruvate kinase M2 silencing was rescued by ectopic expression of p65. Interestingly, pyruvate kinase M2 highly expressed in colorectal cancer tissue, which is correction with macrophage distribution. Taken together, we revealed a novel mechanism of pyruvate kinase M2 in promoting colorectal cancer progression by recruitment of macrophages through p65 nuclear factor-κB-mediated expression of CCL2.

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CCL2-induced chemokine cascade promotes breast cancer metastasis by enhancing retention of metastasis-associated macrophages

Cited by 536 publications

References 58 publications

Cancer immunosurveillance: role of patrolling monocytes

Cancer immunosurveillance: role of patrolling monocytes

Benzopyrene promotes lung cancer A549 cell migration and invasion through up-regulating cytokine IL8 and chemokines CCL2 and CCL3 expression

Specific tumor-derived CCL2 mediated by pyruvate kinase M2 in colorectal cancer cells contributes to macrophage recruitment in tumor microenvironment

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