scholarly journals Tumor-Associated Macrophages and Neutrophils in Tumor Microenvironment

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Jaehong Kim ◽  
Jong-Sup Bae
Keyword(s):  
Tumor Microenvironment ◽  
Immune Cells ◽  
Immune Surveillance ◽  
Tumor Cell Invasion ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Invasion And Metastasis ◽  
Tumor Associated Macrophages ◽  
Tumor Tissues ◽  
Tumor Associated Neutrophils

Distinct tumor microenvironment forms in each progression step of cancer and has diverse capacities to induce both adverse and beneficial consequences for tumorigenesis. It is now known that immune cells can be activated to favor tumor growth and progression, most probably influenced by the tumor microenvironment. Tumor-associated macrophages and tumor-associated neutrophils can exert protumoral functions, enhancing tumor cell invasion and metastasis, angiogenesis, and extracellular matrix remodeling, while inhibiting the antitumoral immune surveillance. Considering that neutrophils in inflammatory environments recruit macrophages and that recruited macrophages affect neutrophil functions, there may be various degrees of interaction between tumor-associated macrophages and tumor-associated neutrophils. Platelets also play an important role in the recruitment and regulation of monocytic and granulocytic cells in the tumor tissues, suggesting that platelet function may be essential for generation of tumor-associated macrophages and tumor-associated neutrophils. In this review, we will explore the biology of tumor-associated macrophages and tumor-associated neutrophils and their possible interactions in the tumor microenvironment. Special attention will be given to the recruitment and activation of these tumor-associated cells and to the roles they play in maintenance of the tumor microenvironment and progression of tumors.

scholarly journals The Role of Tumor-Associated Macrophages in Colorectal Carcinoma Progression

2018 ◽  
Vol 45 (1) ◽  
pp. 356-365 ◽  
Author(s):  
Xiaoming Zhong ◽  
Bin Chen ◽  
Zhiwen Yang
Keyword(s):  
Extracellular Matrix ◽  
Tumor Microenvironment ◽  
Colorectal Carcinoma ◽  
Tumor Growth ◽  
Immune Cells ◽  
Strong Evidence ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Tumor Associated Macrophages

Tumor-associated macrophages (TAMs) are one of the most abundant immune cells in the tumor microenvironment, and they play a pivotal role in prompting the various tumor growth. However, the role of TAMs in colorectal carcinoma (CRC) is controversial, because a few papers report that TAMs is beneficial to CRC patients. In this review, we discuss the good or bad roles of TAMs in CRC progression. Interestingly, recent studies provide strong evidence that TAMs facilitate CRC growth, but do not exert tumor suppressive activities. TAMs can stimulate CRC growth by altering extracellular matrix remodeling, tumor metabolism, angiogenesis, as well as the tumor microenvironment. Therefore, TAMs could serve as a target for CRC therapeutic treatment.

scholarly journals Tumor-Associated Neutrophils and Macrophages—Heterogenous but Not Chaotic

2020 ◽  
Vol 11 ◽  
Author(s):  
Ling Wu ◽  
Xiang H.-F. Zhang
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Progression ◽  
Cancer Cells ◽  
Immune Cells ◽  
Mutual Influence ◽  
Therapeutic Resistance ◽  
Tumor Associated Macrophages ◽  
Tumor Associated Neutrophils ◽  
Shed Light ◽  
Lines Of Evidence

Tumor-associated macrophages (TAMs) and tumor-associated neutrophils (TANs) have been extensively studied. Their pleotropic roles were observed in multiple steps of tumor progression and metastasis, and sometimes appeared to be inconsistent across different studies. In this review, we collectively discussed many lines of evidence supporting the mutual influence between cancer cells and TAMs/TANs. We focused on how direct interactions among these cells dictate co-evolution involving not only clonal competition of cancer cells, but also landscape shift of the entire tumor microenvironment (TME). This co-evolution may take distinct paths and contribute to the heterogeneity of cancer cells and immune cells across different tumors. A more in-depth understanding of the cancer-TAM/TAN co-evolution will shed light on the development of TME that mediates metastasis and therapeutic resistance.

scholarly journals 4-Methylumbelliferone Attenuates Macrophage Invasion and Myocardial Remodeling in Pressure-Overloaded Mouse Hearts

Hypertension ◽  
2021 ◽  
Author(s):  
Katarzyna Hackert ◽  
Susanne Homann ◽  
Shakila Mir ◽  
Arne Beran ◽  
Simone Gorreßen ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Hyaluronic Acid ◽  
Immune Cells ◽  
Inflammatory Responses ◽  
Pressure Overload ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Cardiac Wall

Cardiac wall stress induces local and systemic inflammatory responses that are increasingly recognized as key modulators of extracellular matrix remodeling. Hyaluronic acid interacts with immune cells and mesenchymal cells thereby modulating profibrotic signals. Here we tested the hypothesis that 4-methylumbelliferone (4-MU), an inhibitor of hyaluronic acid synthesis, would attenuate inflammation and extracellular matrix remodeling of pressure-overloaded myocardium in C57BL/6J male mice fed with 4-MU and subjected to TAC (transverse aortic constriction) surgery. Flow cytometry of immune cells showed TAC-induced leukocytosis due to an increase of neutrophils and monocytes. 4-MU strongly attenuated both circulating and cardiac leukocyte numbers 3 days after TAC. In the hearts, 4-MU reduced the number of CCR2 − resident macrophages. At later time points, 4-MU also prevented the infiltration of heart tissue by bone marrow-derived circulating monocytes leading to reduced cardiac macrophage counts even 7 weeks after TAC. The long-term attenuation of macrophage-driven inflammation was associated with less myocardial fibrosis in 4-MU-treated compared with untreated mice. Unexpectedly, 4-MU also reduced the development of left ventricular hypertrophy and increased cardiac output after TAC without affecting blood pressure. The data demonstrate that 4-MU reduces both resident and invading cardiac macrophages and may be a promising agent to alleviate pressure-overload induced myocardial damage.

scholarly journals Theranostic Probes for Targeting Tumor Microenvironment: An Overview

2017 ◽  
Author(s):  
Musafar Gani Sikkandhar ◽  
Anu Maashaa Nedumaran ◽  
Roopa Ravichandar ◽  
Satnam Singh ◽  
Induja Santhakumar ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Immune Cells ◽  
Nuclear Imaging ◽  
Future Perspective ◽  
Resonance Imaging ◽  
Invasion And Metastasis ◽  
Connective Tissues ◽  
Anticancer Drug Delivery ◽  
Promote Tumor Growth ◽  
Magnetic Resonance Imaging Mri

Long gone was the time when tumors were thought to be insular masses of cells, residing independently at specific sites in an organ. Now, researchers gradually realize that tumors interact with the extracellular matrix (ECM), blood vessels, connective tissues and immune cells in their environment, which is now known as the tumor microenvironment (TME). It is found that the interactions between tumors and their surrounding promote tumor growth, invasion and metastasis. The dynamics and diversity of TME cause the tumors to be heterogeneous and thus pose a challenge for cancer diagnosis, drug design and therapy. As TME is significant in enhancing tumor progression, it is vital to identify the different components in the TME. This review explores how different factors in the TME supply tumors with the required growth factors and signaling molecules to proliferate, invade and metastasis. We also examine the development of TME-targeted nanotheranostics over the recent years for cancer therapy, diagnosis and anticancer drug delivery system. This review further discusses the limitations and future perspective of nanoparticle based theranostics when used in combination with current imaging modalities like Optical Imaging, Magnetic Resonance Imaging (MRI) and Nuclear Imaging (PET and SPECT).

scholarly journals Tumor Extracellular Matrix Remodeling: New Perspectives as a Circulating Tool in the Diagnosis and Prognosis of Solid Tumors

Cells ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 81 ◽  
Author(s):  
Marta Giussani ◽  
Tiziana Triulzi ◽  
Gabriella Sozzi ◽  
Elda Tagliabue
Keyword(s):  
Extracellular Matrix ◽  
Tumor Microenvironment ◽  
Tumor Tissue ◽  
Prognostic Markers ◽  
Complex Mixture ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Ecm Remodeling ◽  
Diagnosis And Prognosis ◽  
Novel Concept

: In recent years, it has become increasingly evident that cancer cells and the local microenvironment are crucial in the development and progression of tumors. One of the major components of the tumor microenvironment is the extracellular matrix (ECM), which comprises a complex mixture of components, including proteins, glycoproteins, proteoglycans, and polysaccharides. In addition to providing structural and biochemical support to tumor tissue, the ECM undergoes remodeling that alters the biochemical and mechanical properties of the tumor microenvironment and contributes to tumor progression and resistance to therapy. A novel concept has emerged, in which tumor-driven ECM remodeling affects the release of ECM components into peripheral blood, the levels of which are potential diagnostic or prognostic markers for tumors. This review discusses the most recent evidence on ECM remodeling-derived signals that are detectable in the bloodstream, as new early diagnostic and risk prediction tools for the most frequent solid cancers.

scholarly journals Role of neutrophil extracellular traps in regulation of lung cancer invasion and metastasis: Structural Insights from a Computational Model

2020 ◽  
Author(s):  
Junho Lee ◽  
Donggu Lee ◽  
Sean Lawler ◽  
Yangjin Kim
Keyword(s):  
Mathematical Model ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Tumor Invasion ◽  
Neutrophil Extracellular Traps ◽  
Tumor Cell Invasion ◽  
Invasion And Metastasis ◽  
Extracellular Traps ◽  
Tumor Associated Neutrophils

AbstractLung cancer is one of the leading causes of cancer-related deaths worldwide and is characterized by hijacking immune system for active growth and aggressive metastasis. Neutrophils, which in their original form should establish immune activities to the tumor as a first line of defense, are undermined by tumor cells to promote tumor invasion in several ways. In this study, we investigate the mutual interactions between the tumor cells and the neutrophils that facilitate tumor invasion by developing a mathematical model that involves taxis-reaction-diffusion equations for the critical components in the interaction. These include the densities of tumor and neutrophils, and the concentrations of signaling molecules and structure such as neutrophil extracellular traps (NETs). We apply the mathematical model to a Boyden invasion assay used in the experiments to demonstrate that the tumor-associated neutrophils can enhance tumor cell invasion by secreting the neutrophil elastase. We show that the model can both reproduce the major experimental observation on NET-mediated cancer invasion and make several important predictions to guide future experiments with the goal of the development of new anti-tumor strategies. Moreover, using this model, we investigate the fundamental mechanism of NET-mediated invasion of cancer cells and the impact of internal and external heterogeneity on the migration patterning of tumour cells and their response to different treatment schedules.Author summaryWhen cancer patients are diagnosed with tumours at a primary site, the cancer cells are often found in the blood or already metastasized to the secondary sites in other organs. These metastatic cancer cells are more resistant to major anti-cancer therapies, and lead to the low survival probability. Until recently, the role of neutrophils, specifically tumor-associated neutrophils as a member of complex tumor microenvironment, has been ignored for a long time due to technical difficulties in tumor biology but these neutrophils are emerging as an important player in regulation of tumor invasion and metastasis. The mutual interaction between a tumor and neutrophils from bone marrow or in blood induces the critical transition of the naive form, called the N1 type, to the more aggressive phenotype, called the N2 TANs, which then promotes tumor invasion. In this article, we investigate how stimulated neutrophils with different N1 and N2 landscapes shape the metastatic potential of the lung cancers. Our simulation framework is designed for boyden invasion chamber in experiments and based on a mathematical model that describes how tumor cells interact with neutrophils and N2 TANs can promote tumor cell invasion. We demonstrate that the efficacy of anti-tumor (anti-invasion) drugs depend on this critical communication and N1 → N2 landscapes of stimulated neutrophils.

scholarly journals Estrogens and the Schrödinger’s Cat in the Ovarian Tumor Microenvironment

Cancers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 5011
Author(s):  
Marija Gjorgoska ◽  
Tea Lanišnik Rižner
Keyword(s):  
Ovarian Cancer ◽  
Tumor Microenvironment ◽  
Tumor Growth ◽  
Immune Cells ◽  
Metabolic Pathways ◽  
Ovarian Tumor ◽  
Cancer Biology ◽  
Thought Experiment ◽  
Invasion And Metastasis ◽  
Established Tumor

Ovarian cancer is a heterogeneous disease affecting the aging ovary, in concert with a complex network of cells and signals, together representing the ovarian tumor microenvironment. As in the “Schrödinger’s cat” thought experiment, the context-dependent constituents of the—by the time of diagnosis—well-established tumor microenvironment may display a tumor‑protective and ‑destructive role. Systemic and locally synthesized estrogens contribute to the formation of a pro-tumoral microenvironment that enables the sustained tumor growth, invasion and metastasis. Here we focus on the estrogen biosynthetic and metabolic pathways in ovarian cancer and elaborate their actions on phenotypically plastic, estrogen-responsive, aging immune cells of the tumor microenvironment, altogether highlighting the multicomponent-connectedness and complexity of cancer, and contributing to a broader understanding of the ovarian cancer biology.

scholarly journals Interplay of Immunometabolism and Epithelial–Mesenchymal Transition in the Tumor Microenvironment

2021 ◽  
Vol 22 (18) ◽  
pp. 9878
Author(s):  
Ming-Yu Chou ◽  
Muh-Hwa Yang
Keyword(s):  
Tumor Microenvironment ◽  
Immune Cells ◽  
Tumor Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Immune Surveillance ◽  
Metabolic Reprogramming ◽  
Mesenchymal Transition ◽  
Regulatory Loop ◽  
The Relationship

Epithelial–mesenchymal transition (EMT) and metabolic reprogramming in cancer cells are the key hallmarks of tumor metastasis. Since the relationship between the two has been well studied, researchers have gained increasing interest in the interplay of cancer cell EMT and immune metabolic changes. Whether the mutual influences between them could provide novel explanations for immune surveillance during metastasis is worth understanding. Here, we review the role of immunometabolism in the regulatory loop between tumor-infiltrating immune cells and EMT. We also discuss the challenges and perspectives of targeting immunometabolism in cancer treatment.

Proinvasive extracellular matrix remodeling in tumor microenvironment in response to radiation

Oncogene ◽  
2018 ◽  
Vol 37 (24) ◽  
pp. 3317-3328 ◽  
Author(s):  
Ki-Chun Yoo ◽  
Yongjoon Suh ◽  
Yoojeong An ◽  
Hae-June Lee ◽  
Ye Ji Jeong ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Tumor Microenvironment ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling

scholarly journals Targeting Tumor-Associated Macrophages in Cancer Immunotherapy

Cancers ◽  
2021 ◽  
Vol 13 (21) ◽  
pp. 5318
Author(s):  
Amy J. Petty ◽  
Dwight H. Owen ◽  
Yiping Yang ◽  
Xiaopei Huang
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Invasion ◽  
Therapeutic Strategies ◽  
Invasion And Metastasis ◽  
Tumor Associated Macrophages ◽  
Leukocyte Population ◽  
Promote Tumor Growth ◽  
Tumor Growth And Metastasis ◽  
Poor Outcomes ◽  
Inhibitory Molecules

Tumor-associated macrophages (TAMs) represent the most abundant leukocyte population in most solid tumors and are greatly influenced by the tumor microenvironment. More importantly, these macrophages can promote tumor growth and metastasis through interactions with other cell populations within the tumor milieu and have been associated with poor outcomes in multiple tumors. In this review, we examine how the tumor microenvironment facilitates the polarization of TAMs. Additionally, we evaluate the mechanisms by which TAMs promote tumor angiogenesis, induce tumor invasion and metastasis, enhance chemotherapeutic resistance, and foster immune evasion. Lastly, we focus on therapeutic strategies that target TAMs in the treatments of cancer, including reducing monocyte recruitment, depleting or reprogramming TAMs, and targeting inhibitory molecules to increase TAM-mediated phagocytosis.

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