Macrophage Polarization: Anti-Cancer Strategies to Target Tumor-Associated Macrophage in Breast Cancer

Tariq, Muhammad; Zhang, Jieqiong; Liang, Guikai; Ding, Ling; He, Qiaojun; Yang, Bo

doi:10.1002/jcb.25895

Cited by 147 publications

(115 citation statements)

References 187 publications

(270 reference statements)

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“…TAMs play an important role in mediating adaptive immune response in cancer. Interestingly, macrophages can have both anti-and proinflammatory roles, which is often linked to their M1 or M2 polarization status (reviewed in Tariq et al, 2017). Various ECM components are involved in TAM polarization: At least in cell culture, HA alone is able to strongly drive macrophage polarization toward a protumorigenic and antiinflammatory M2 phenotype (Kim et al, 2019).…”

Section: Effects Of the Ecm On Immunotherapymentioning

confidence: 99%

Extracellular Matrix in the Tumor Microenvironment and Its Impact on Cancer Therapy

Henke

Nandigama

Ergün

2020

Front. Mol. Biosci.

646

522

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Solid tumors are complex organ-like structures that consist not only of tumor cells but also of vasculature, extracellular matrix (ECM), stromal, and immune cells. Often, this tumor microenvironment (TME) comprises the larger part of the overall tumor mass. Like the other components of the TME, the ECM in solid tumors differs significantly from that in normal organs. Intratumoral signaling, transport mechanisms, metabolisms, oxygenation, and immunogenicity are strongly affected if not controlled by the ECM. Exerting this regulatory control, the ECM does not only influence malignancy and growth of the tumor but also its response toward therapy. Understanding the particularities of the ECM in solid tumor is necessary to develop approaches to interfere with its negative effect. In this review, we will also highlight the current understanding of the physical, cellular, and molecular mechanisms by which the pathological tumor ECM affects the efficiency of radio-, chemo-, and immunotherapy. Finally, we will discuss the various strategies to target and modify the tumor ECM and how they could be utilized to improve response to therapy.

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Section: Effects Of the Ecm On Immunotherapymentioning

confidence: 99%

Extracellular Matrix in the Tumor Microenvironment and Its Impact on Cancer Therapy

Henke

Nandigama

Ergün

2020

Front. Mol. Biosci.

646

522

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“…Moreover, even at 10 weeks after DMBA/TPA treatment, intradermal macrophage recruitment was attenuated in Cx3cr1 -/- mice, compared to the case in WT mice (Figure 3, C and D). Given the important role of macrophage polarization to M2-like phenotype in carcinogenesis (Tariq et al , 2017; Isidro & Appleyard, 2016), we determined the expression of M2-related molecules in dermal macrophages isolated from DMBA/TPA-treated WT or Cx3cr1 -/- mice. The numbers of the isolated whole macrophages were significantly reduced in Cx3cr1 -/- mice, compared to the WT mice, both at 48 and 72 h after DMBA/TPA treatment (Figure 3E).…”

Section: Resultsmentioning

confidence: 99%

Pivotal involvement of the CX3CL1-CX3CR1 axis for the recruitment of M2-TAMs in skin carcinogenesis

Ishida

Kuninaka

Yamamoto

et al. 2019

Preprint

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24We previously revealed the crucial roles of CX3CL1-CX3CR1 axis in skin wound 25 healing. Although repeated wounds frequently develop into skin cancer, the roles of 26 CX3CL1 in skin carcinogenesis remain elusive. Here, we proved that CX3CL1 protein 27 expression and CX3CR1 + macrophages were observed in human skin cancer tissues. 28 Similarly, we observed the enhancement of CX3CL1 expression and the abundant 29 accumulation of CX3CR1 + tumor-associated macrophages (TAMs) with M2 phenotypes 30 in the skin carcinogenesis process induced by the combined treatment with 31 7,12-dimethylbenz-(a)anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate 32 (TPA). In this mouse skin carcinogenesis process, CX3CR1 + TAMs exhibited M2 33 phenotypes with the expression of Wnt3a and angiogenic molecules including vascular 34 endothelial growth factor (VEGF) and matrix metalloproteinase (MMP)-9. Compared to 35 wild-type mice, CX3CR1-deficient mice showed fewer numbers of skin tumors with a 36 lower incidence. Concomitantly, M2-macrophage numbers and neovascularization 37 reduced with the depressed expression of angiogenic factors and Wnt3a. Thus, the 38 CX3CL1-CX3CR1 axis can crucially contribute to skin carcinogenesis by regulating the 39 accumulation and functions of TAMs. Thus, this axis can be a good target for preventing 40 and/or treating skin cancers. 41 42 43 Ishida et al. 3 3

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“…ERK signaling was reported to participate in EMT transcription factors mediated downregulation of Ecadherin in cancers [20][21][22] . In Fig.…”

Section: Rage Downregulates E-cadherin Expression Through Erk1/ 2-depmentioning

confidence: 99%

“…Since the in vivo data of tumor growth were inconsistent with in vitro, which factors promoted the in vivo tumor growth in RAGE-overexpressed groups were further evaluated. Tumor-associated macrophages (TAMs) in tumor microenvironment (TME) are responsible for the development and progression of tumor [19][20][21] . To evaluate the effect of RAGE on the recruitment of TAMs in vivo, the expression profile of TAM markers CD68 and CD163 [22][23][24] in the inoculated tumors was evaluated by IHC assay.…”

Section: Rage Modulates the Tumor Microenvironment In A Xenograft Animentioning

confidence: 99%

RAGE acts as an oncogenic role and promotes the metastasis of human lung cancer

Chen

Chang

et al. 2020

Cell Death Dis

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RAGE (receptor for advanced glycation end-product) is thought to be associated with metastasis and poor prognosis of various types of cancer. However, RAGE is constitutively expressed in the normal lung and down-regulated in cancerous lung, while the opposite evidence shows that RAGE-mediated signaling contributes to the tumorigenesis of lung cancer. Therefore, the role of RAGE in lung cancer progression is still unclear to be further investigated. In this study, RAGE-overexpressed stable clones of human lung cancer A549 cells and two local lung adenocarcinoma cell lines CL1-0 and CL1-5 were utilized to verify the effect of RAGE on lung cancer cells while the in vivo xenograft animal model was further performed to evaluate the role of RAGE in the progression of lung cancer. The growth of A549 cells was inhibited by RAGE overexpression. p53-dependent p21 CIP1 expression contributed to RAGE-induced growth inhibition by suppressing CDK2 kinase activity and retinoblastoma protein (RB) phosphorylation in vitro. On the other hand, RAGE overexpression promoted migration, invasion, and mesenchymal features of lung adenocarcinoma cells through ERK signaling. Furthermore, an in vivo xenograft experiment indicated that RAGE promoted the metastasis of lung cancer cells with p21 CIP1 up-regulation, ERK activation, and the changes of EMT markers. Regarding to the involvement of tumor-associated macrophage (TAM) in the microenvironment, we monitored the expressions of TAM markers including CD68 and CD163 as well as angiogenesis marker CD31 in xenograft slice. The data showed that RAGE might induce the accumulation of TAM in lung cancer cells and further accelerate the in vivo tumor growth. In summary, our study provides evidence indicating the distinct in vitro and in vivo effects of RAGE and related mechanisms on tumor growth and metastasis, which shed light on the oncogenic role of RAGE in lung cancer.

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Macrophage Polarization: Anti-Cancer Strategies to Target Tumor-Associated Macrophage in Breast Cancer

Cited by 147 publications

References 187 publications

Extracellular Matrix in the Tumor Microenvironment and Its Impact on Cancer Therapy

Extracellular Matrix in the Tumor Microenvironment and Its Impact on Cancer Therapy

Pivotal involvement of the CX3CL1-CX3CR1 axis for the recruitment of M2-TAMs in skin carcinogenesis

RAGE acts as an oncogenic role and promotes the metastasis of human lung cancer

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