Tumor-associated macrophages: an effective player of the tumor microenvironment

Abstract

Cancer progression is primarily caused by interactions between transformed cells and the components of the tumor microenvironment (TME). TAMs (tumor-associated macrophages) make up the majority of the invading immune components, which are further categorized as anti-tumor M1 and pro-tumor M2 subtypes. While M1 is known to have anti-cancer properties, M2 is recognized to extend a protective role to the tumor. As a result, the tumor manipulates the TME in such a way that it induces macrophage infiltration and M1 to M2 switching bias to secure its survival. This M2-TAM bias in the TME promotes cancer cell proliferation, neoangiogenesis, lymphangiogenesis, epithelial-to-mesenchymal transition, matrix remodeling for metastatic support, and TME manipulation to an immunosuppressive state. TAMs additionally promote the emergence of cancer stem cells (CSCs), which are known for their ability to originate, metastasize, and relapse into tumors. CSCs also help M2-TAM by revealing immune escape and survival strategies during the initiation and relapse phases. This review describes the reasons for immunotherapy failure and, thereby, devises better strategies to impair the tumor–TAM crosstalk. This study will shed light on the understudied TAM-mediated tumor progression and address the much-needed holistic approach to anti-cancer therapy, which encompasses targeting cancer cells, CSCs, and TAMs all at the same time.

Irradiated microparticles suppress prostate cancer by tumor microenvironment reprogramming and ferroptosis

“…Macrophages are also APCs and function to activate T cells. However, tumor-associated macrophages (TAMs) always act as promoters of tumor progression by secreting anti-inflammatory cytokines such as IL-10 and TGF-β [ 20 , 38 ]. Therefore, we measured the direct influence of RC@RMPs on APCs to evaluate the effect that RC@RMPs may have on reshaping the immunological environment of the tumor.…”

Overnutrition and Lipotoxicity: Impaired Efferocytosis and Chronic Inflammation as Precursors to Multifaceted Disease Pathogenesis

“…Foam cells are found in atherosclerotic plaques, where they can accumulate lipid droplets and exhibit impaired efferocytosis due to lipid overload, contributing to plaque instability and inflammation [80]. Tumor-associated macrophages (TAMs) are present within tumor microenvironments, and they demonstrate impaired efferocytosis, promoting tumor progression and immune evasion [81]. Peritoneal macrophages inhabit the peritoneal cavity, and compromised efferocytosis due to these macrophages is a factor in conditions such as peritonitis and inflammatory disorders affecting the abdomen [82].…”

Inhibition of MMP-2 and MMP-9 by Dietary Antioxidants in THP-1 Macrophages and Sera from Patients with Breast Cancer

“…It is now known that inflammation plays a key role in tumor development and progression and that these processes are driven by a complex interplay between malignant tumor cells and the surrounding nonmalignant stroma, comprising the extracellular matrix (ECM); stromal cells such as endothelial cells (ECs); fibroblasts; and infiltrating immune cells. Among infiltrated immune cells, tumor-associated macrophages (TAMs) represent the primary resident cells of the breast tumor microenvironment (TME) and are the main cells implicated in inflammatory processes [4] via their ability to secrete inflammatory factors such as pro-inflammatory cytokines and matrix metalloproteinases (MMPs) [5,6].…”