Cancer-associated fibroblasts enhance tumor-associated macrophages enrichment and suppress NK cells function in colorectal cancer

Zhang, Rongsheng; Qi, Fan; Zhao, Fei; Li, Geng; Shao, Shui-jin; Zhang, Xiaochao; Yuan, Lin; Feng, Yongdong

doi:10.1038/s41419-019-1435-2

Cited by 232 publications

(212 citation statements)

References 38 publications

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“…Tumor-associated macrophage TAM is another key element of the TME which significantly affects cancer cell behavior [87]. Similar to CAFs, TAMs are heterogeneous and available in different types depending on their origin and function [88].…”

Section: Cancer-associated Fibroblast (Cafs)mentioning

confidence: 99%

Tumor microenvironment complexity and therapeutic implications at a glance

et al. 2020

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The dynamic interactions of cancer cells with their microenvironment consisting of stromal cells (cellular part) and extracellular matrix (ECM) components (non-cellular) is essential to stimulate the heterogeneity of cancer cell, clonal evolution and to increase the multidrug resistance ending in cancer cell progression and metastasis. The reciprocal cell-cell/ECM interaction and tumor cell hijacking of non-malignant cells force stromal cells to lose their function and acquire new phenotypes that promote development and invasion of tumor cells. Understanding the underlying cellular and molecular mechanisms governing these interactions can be used as a novel strategy to indirectly disrupt cancer cell interplay and contribute to the development of efficient and safe therapeutic strategies to fight cancer. Furthermore, the tumor-derived circulating materials can also be used as cancer diagnostic tools to precisely predict and monitor the outcome of therapy. This review evaluates such potentials in various advanced cancer models, with a focus on 3D systems as well as lab-on-chip devices.

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Section: Cancer-associated Fibroblast (Cafs)mentioning

confidence: 99%

Tumor microenvironment complexity and therapeutic implications at a glance

et al. 2020

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“…67 Furthermore, the synergetic effects of CAFs and TAMs, which induced by CAFs increasing the suppression of NK cells functions in colorectal cancer. 67 In addition, CAFs significantly suppressed the cytotoxicity function of NK cells via releasing PGE2 in melanoma. 68 In the presence of NK cells, the CAF-induced expression of PGE2 was higher than fibroblasts, 64 suggesting that NK cells can also influence the cytokine expression of CAFs.…”

Section: Interaction Between Cancer-associated Fibroblasts and Mastmentioning

confidence: 99%

Crosstalk between cancer‐associated fibroblasts and immune cells in cancer

Liu

Chen

et al. 2019

J Cellular Molecular Medi

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Multiple studies have shown that cancer‐associated fibroblasts (CAFs) play an important role in tumour progression, including carcinogenesis, invasion, metastasis and the chemoresistance of cancer cells. Immune cells, including macrophages, natural killer cells, dendritic cells and T cells, play a dual role in the tumour microenvironment. Although increasing research has focused on studying interactions between distinct cells in the tumour microenvironment, the complex relationships between CAFs and immune cells remain unclear and need further study. Here, we summarize our current understanding of crosstalk between CAFs and immune cells, which may help clarify their diagnostic and therapeutic value in tumour progression.

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“…The progression of glioma involves the role of interconnected glioma cells and TAMs in the tumor microenvironment [33]. This increase in in ltrates is connected to the poor prognosis ofglioma [5].…”

Section: Discussionmentioning

confidence: 99%

SETDB1 Promotes the Growth of Glioma via CSF-1-dependent Macrophage Recruitment by Activating the AKT/mTOR Signaling Pathway

Han

Wei

Guo

et al. 2020

Preprint

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Background: Glioma is a common disease of the central nervous system (CNS), with high morbidity and mortality. Among the infiltrates in the tumor microenvironment, tumor-associated macrophages (TAMs) are abundant and they are significant factors in glioma progression. However, the exact details of disease progression have yet to be determined. Methods: The clinical relevance of SETDB1 was analyzed by immunohistochemistry, real-time PCR and Western blotting and of glioma cancer tissues. Tumor cell proliferation, migration and invasion were investigated by MTS assay, colony formation assay, xenograft, wound healing and Transwell assay. The relationship between SETDB1 and CSF-1, as well as TAMS was examined by Western blotting, real-time PCR and syngeneic mouse model.Results: This work shows the presence and upregulation of SETDB1 in gliomaand its relationship with disease prognosis. Gain and loss of function approaches showed the inhibition of apoptosis and the promotion of growth, migration and invasion of the disease with SETDB1 overexpression and converse effects with SETDB1 silencing in vitro. Mechanistically, SETDB1 promotes CSF-1 expression by activating the AKT/mTOR signaling pathway. This leads to macrophage recruitment in the tumor, leading to tumor growth. Conclusion: This studyclarifies the modulation of tumor functions by SETDB1 and hence presents a future avenue for treating glioma.

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Cancer-associated fibroblasts enhance tumor-associated macrophages enrichment and suppress NK cells function in colorectal cancer

Cited by 232 publications

References 38 publications

Tumor microenvironment complexity and therapeutic implications at a glance

Tumor microenvironment complexity and therapeutic implications at a glance

Crosstalk between cancer‐associated fibroblasts and immune cells in cancer

SETDB1 Promotes the Growth of Glioma via CSF-1-dependent Macrophage Recruitment by Activating the AKT/mTOR Signaling Pathway

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