Tumor microenvironment, histone modifications, and myeloid-derived suppressor cells

Tian, Xinyu; Wang, Ting; Shen, Han; Wang, Shengjun

doi:10.1016/j.cytogfr.2023.08.002

Cited by 8 publications

(3 citation statements)

References 120 publications

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“…The ECM is a key constitutive part of the TME, consisting principally of reactive tissue components including glycoproteins, collagens, and many enzymes that have an impact on cell adhesion, proliferation, and communication. These substances can change their physical properties, composition, and the environment in which they live to affect tumor cell migration, while the concentration of ECM also determines the ratio of tumor cell migration from one region to another (72)(73)(74)(75)(76). Additionally, nonmalignant cells in the TME are prominently separated into two primary groups, immune cells and mesenchymal stromal cells, which stimulate and promote uncontrolled cell proliferation to affect all stages of carcinogenesis (77)(78)(79).…”

Section: The Overview Of Tamsmentioning

confidence: 99%

Exosome-mediated communication between gastric cancer cells and macrophages: implications for tumor microenvironment

Qiu,

Lu,

et al. 2024

Front. Immunol.

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Gastric cancer (GC) is a malignant neoplasm originating from the epithelial cells of the gastric mucosa. The pathogenesis of GC is intricately linked to the tumor microenvironment within which the cancer cells reside. Tumor-associated macrophages (TAMs) primarily differentiate from peripheral blood monocytes and can be broadly categorized into M1 and M2 subtypes. M2-type TAMs have been shown to promote tumor growth, tissue remodeling, and angiogenesis. Furthermore, they can actively suppress acquired immunity, leading to a poorer prognosis and reduced tolerance to chemotherapy. Exosomes, which contain a myriad of biologically active molecules including lipids, proteins, mRNA, and noncoding RNAs, have emerged as key mediators of communication between tumor cells and TAMs. The exchange of these molecules via exosomes can markedly influence the tumor microenvironment and consequently impact tumor progression. Recent studies have elucidated a correlation between TAMs and various clinicopathological parameters of GC, such as tumor size, differentiation, infiltration depth, lymph node metastasis, and TNM staging, highlighting the pivotal role of TAMs in GC development and metastasis. In this review, we aim to comprehensively examine the bidirectional communication between GC cells and TAMs, the implications of alterations in the tumor microenvironment on immune escape, invasion, and metastasis in GC, targeted therapeutic approaches for GC, and the efficacy of potential GC drug resistance strategies.

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Section: The Overview Of Tamsmentioning

confidence: 99%

Exosome-mediated communication between gastric cancer cells and macrophages: implications for tumor microenvironment

Qiu,

Lu,

et al. 2024

Front. Immunol.

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show abstract

“…Nevertheless, the killing activity of T cells is hindered by the accumulation of TGF-β in the TME, and the antigen-presenting function of DCs is impaired by the hypoxic and inflammatory conditions of the TME ( 46 , 47 ). Additionally, MDSCs, acting as negative immune regulators within the TME, suppress T-cell activation and the functions of various immune cells ( 48 , 49 ).…”

Section: Overview Of the Tmementioning

confidence: 99%

Recent advances in understanding the immune microenvironment in ovarian cancer

Chen,

Yang,

et al. 2024

Front. Immunol.

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The occurrence of ovarian cancer (OC) is a major factor in women’s mortality rates. Despite progress in medical treatments, like new drugs targeting homologous recombination deficiency, survival rates for OC patients are still not ideal. The tumor microenvironment (TME) includes cancer cells, fibroblasts linked to cancer (CAFs), immune-inflammatory cells, and the substances these cells secrete, along with non-cellular components in the extracellular matrix (ECM). First, the TME mainly plays a role in inhibiting tumor growth and protecting normal cell survival. As tumors progress, the TME gradually becomes a place to promote tumor cell progression. Immune cells in the TME have attracted much attention as targets for immunotherapy. Immune checkpoint inhibitor (ICI) therapy has the potential to regulate the TME, suppressing factors that facilitate tumor advancement, reactivating immune cells, managing tumor growth, and extending the survival of patients with advanced cancer. This review presents an outline of current studies on the distinct cellular elements within the OC TME, detailing their main functions and possible signaling pathways. Additionally, we examine immunotherapy rechallenge in OC, with a specific emphasis on the biological reasons behind resistance to ICIs.

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“…Studies have shown that histone modifications contribute to the accumulation and function of MDSCs [ 255 , 256 , 257 ]. Analysis of CRC tissues revealed that HDAC related genes were up‐regulated in tumor‐infiltrating immature‐MDSC (I‐MDSC), while HAT‐related genes were down‐regulated in CRC patients.…”

Section: Mechanisms In Iscsmentioning

confidence: 99%

Converting “cold” to “hot”: epigenetics strategies to improve immune therapy effect by regulating tumor‐associated immune suppressive cells

Tang,

Cui,

Liu

et al. 2024

Cancer Communications

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Significant developments in cancer treatment have been made since the advent of immune therapies. However, there are still some patients with malignant tumors who do not benefit from immunotherapy. Tumors without immunogenicity are called “cold” tumors which are unresponsive to immunotherapy, and the opposite are “hot” tumors. Immune suppressive cells (ISCs) refer to cells which can inhibit the immune response such as tumor‐associated macrophages (TAMs), myeloid‐derived suppressor cells (MDSCs), regulatory T (Treg) cells and so on. The more ISCs infiltrated, the weaker the immunogenicity of the tumor, showing the characteristics of “cold” tumor. The dysfunction of ISCs in the tumor microenvironment (TME) may play essential roles in insensitive therapeutic reaction. Previous studies have found that epigenetic mechanisms play an important role in the regulation of ISCs. Regulating ISCs may be a new approach to transforming “cold” tumors into “hot” tumors. Here, we focused on the function of ISCs in the TME and discussed how epigenetics is involved in regulating ISCs. In addition, we summarized the mechanisms by which the epigenetic drugs convert immunotherapy‐insensitive tumors into immunotherapy‐sensitive tumors which would be an innovative tendency for future immunotherapy in “cold” tumor.

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Tumor microenvironment, histone modifications, and myeloid-derived suppressor cells

Cited by 8 publications

References 120 publications

Exosome-mediated communication between gastric cancer cells and macrophages: implications for tumor microenvironment

Exosome-mediated communication between gastric cancer cells and macrophages: implications for tumor microenvironment

Recent advances in understanding the immune microenvironment in ovarian cancer

Converting “cold” to “hot”: epigenetics strategies to improve immune therapy effect by regulating tumor‐associated immune suppressive cells

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