Tissue-resident macrophages are major tumor-associated macrophage resources, contributing to early TNBC development, recurrence, and metastases

Hirano, Ryuichiro; Okamoto, Koki; Shinke, Miyu; Sato, Marika; Watanabe, S.; Watanabe, Hidenobu; Kondoh, Gen; Kadonosono, Tetsuya; Kizaka‐Kondoh, Shinae

doi:10.1038/s42003-023-04525-7

Cited by 21 publications

(12 citation statements)

References 65 publications

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“…For instance, in early-stage TNBC, TRMs are the primary TAMs. 45 A similar pattern is seen in glioblastoma multiforme (GBM); in newly diagnosed cases, microglia dominate, but in recurrent glioblastoma, MDMs outweigh microglia, especially in hypoxic areas. 62 In IDH mutant gliomas, microglia are predominant, whereas, in IDH wild-type gliomas, the situation is reversed with MDMs surpassing the microglia.…”

Section: The Immune Landscape In the Tumor Microenvironmentmentioning

confidence: 81%

“…In triple-negative breast cancer (TNBC), depletion of TRMs significantly reduces tumor growth, recurrence, and metastasis. 45 In pancreatic ductal adenocarcinoma (PDAC), TRMs promote tissue fibrosis and shape the pro-tumor extracellular matrix. 46 Such evidence indicates that there remain many disputes regarding the roles and mechanisms of TRMs in tumors.…”

Section: The Immune Landscape In the Tumor Microenvironmentmentioning

confidence: 99%

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Harnessing innate immune pathways for therapeutic advancement in cancer

Hu,

Sun,

Lin

et al. 2024

Sig Transduct Target Ther

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The innate immune pathway is receiving increasing attention in cancer therapy. This pathway is ubiquitous across various cell types, not only in innate immune cells but also in adaptive immune cells, tumor cells, and stromal cells. Agonists targeting the innate immune pathway have shown profound changes in the tumor microenvironment (TME) and improved tumor prognosis in preclinical studies. However, to date, the clinical success of drugs targeting the innate immune pathway remains limited. Interestingly, recent studies have shown that activation of the innate immune pathway can paradoxically promote tumor progression. The uncertainty surrounding the therapeutic effectiveness of targeted drugs for the innate immune pathway is a critical issue that needs immediate investigation. In this review, we observe that the role of the innate immune pathway demonstrates heterogeneity, linked to the tumor development stage, pathway status, and specific cell types. We propose that within the TME, the innate immune pathway exhibits multidimensional diversity. This diversity is fundamentally rooted in cellular heterogeneity and is manifested as a variety of signaling networks. The pro-tumor effect of innate immune pathway activation essentially reflects the suppression of classical pathways and the activation of potential pro-tumor alternative pathways. Refining our understanding of the tumor’s innate immune pathway network and employing appropriate targeting strategies can enhance our ability to harness the anti-tumor potential of the innate immune pathway and ultimately bridge the gap from preclinical to clinical application.

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Section: The Immune Landscape In the Tumor Microenvironmentmentioning

confidence: 81%

Section: The Immune Landscape In the Tumor Microenvironmentmentioning

confidence: 99%

Harnessing innate immune pathways for therapeutic advancement in cancer

Hu,

Sun,

Lin

et al. 2024

Sig Transduct Target Ther

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“…Data from human tissue, mouse tissue, and spheroid models indicate that in non-small cell lung carcinoma (NSCLC), tissue-resident macrophages are essential for establishing a TME for the early development of cancer lesions ( Casanova-Acebes et al, 2021 ). Similarly, tissue-resident macrophages in BC are crucial for the early development of triple-negative tumors before angiogenesis ( Hirano et al, 2023 ). Furthermore, the macrophages within pre-malignant lesions promote early dissemination of cancer cells and later metastasis, contributing to disease progression ( Linde et al, 2018 ; Hirano et al, 2023 ).…”

Section: Cross-talk Of Cafs and Tme Cellsmentioning

confidence: 99%

“…Similarly, tissue-resident macrophages in BC are crucial for the early development of triple-negative tumors before angiogenesis ( Hirano et al, 2023 ). Furthermore, the macrophages within pre-malignant lesions promote early dissemination of cancer cells and later metastasis, contributing to disease progression ( Linde et al, 2018 ; Hirano et al, 2023 ). Overall, the available data indicate that tissue-resident macrophages are likely essential in the initial phases of tumor formation, with monocyte-derived macrophages dominating later in tumor development.…”

Section: Cross-talk Of Cafs and Tme Cellsmentioning

confidence: 99%

Dynamic interactions in the tumor niche: how the cross-talk between CAFs and the tumor microenvironment impacts resistance to therapy

Piwocka,

Piotrowski,

Suchorska

et al. 2024

Front. Mol. Biosci.

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The tumor microenvironment (TME) is a complex ecosystem of cells, signaling molecules, and extracellular matrix components that profoundly influence cancer progression. Among the key players in the TME, cancer-associated fibroblasts (CAFs) have gained increasing attention for their diverse and influential roles. CAFs are activated fibroblasts found abundantly within the TME of various cancer types. CAFs contribute significantly to tumor progression by promoting angiogenesis, remodeling the extracellular matrix, and modulating immune cell infiltration. In order to influence the microenvironment, CAFs engage in cross-talk with immune cells, cancer cells, and other stromal components through paracrine signaling and direct cell-cell interactions. This cross-talk can result in immunosuppression, tumor cell proliferation, and epithelial-mesenchymal transition, contributing to disease progression. Emerging evidence suggests that CAFs play a crucial role in therapy resistance, including resistance to chemotherapy and radiotherapy. CAFs can modulate the tumor response to treatment by secreting factors that promote drug efflux, enhance DNA repair mechanisms, and suppress apoptosis pathways. This paper aims to understand the multifaceted functions of CAFs within the TME, discusses cross-talk between CAFs with other TME cells, and sheds light on the contibution of CAFs to therapy resistance. Targeting CAFs or disrupting their cross-talk with other cells holds promise for overcoming drug resistance and improving the treatment efficacy of various cancer types.

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“…In addition to the autonomous changes of autocrine soluble factors [161], the interaction with stromal cells, such as myeloid cells [macrophages, myeloid-derived suppressor cells (MDSCs), and neutrophils], pericytes, fibroblasts, and vascular endothelial cells via growth factors, cytokines, and chemokines plays a crucial role in recurrent tumor formation [13,24,160]. For example, tissue-resident macrophages in the mammary gland are a major source of tumor-associated macrophages and mediate local recurrence and distal metastasis of triple-negative breast cancer (TNBC) [162].…”

Section: Awakening Of Dormant Cancer Cellsmentioning

confidence: 99%

Cellular Dormancy in Cancer: Mechanisms and Potential Targeting Strategies

Min¹,

Lee²

2023

Cancer Res Treat

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Cancer is a leading cause of disease-related mortality worldwide. Drug resistance is one of the primary reasons for the failure of anticancer therapy. There are a number of underlying mechanisms for anticancer drug resistance including genetic/epigenetic modifications, microenvironmental factors, and tumor heterogeneity. In the present scenario, researchers have focused on these novel mechanisms and strategies to tackle them. Recently, researchers have recognized the ability of cancer to become dormant because of anticancer drug resistance, tumor relapse, and progression. Currently, cancer dormancy is classified into "tumor mass dormancy" and "cellular dormancy." Tumor mass dormancy represents the equilibrium between cell proliferation and cell death under the control of blood supply and immune responses. Cellular dormancy denotes the state in which cells undergo quiescence and is characterized by autophagy, stress-tolerance signaling, microenvironmental cues, and epigenetic modifications. Cancer dormancy has been regarded as the stem of primary or distal recurrent tumor formation and poor clinical outcomes in cancer patients. Despite the insufficiency of reliable models of cellular dormancy, the mechanisms underlying the regulation of cellular dormancy have been clarified in numerous studies. A better understanding of the biology of cancer dormancy is critical for the development of effective anticancer therapeutic strategies. In this review, we summarize the characteristics and regulatory mechanisms of cellular dormancy, introduce several potential strategies for targeting cellular dormancy, and discuss future perspectives.

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Tissue-resident macrophages are major tumor-associated macrophage resources, contributing to early TNBC development, recurrence, and metastases

Cited by 21 publications

References 65 publications

Harnessing innate immune pathways for therapeutic advancement in cancer

Harnessing innate immune pathways for therapeutic advancement in cancer

Dynamic interactions in the tumor niche: how the cross-talk between CAFs and the tumor microenvironment impacts resistance to therapy

Cellular Dormancy in Cancer: Mechanisms and Potential Targeting Strategies

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