Taraxacum mongolicum extract inhibited malignant phenotype of triple-negative breast cancer cells in tumor-associated macrophages microenvironment through suppressing IL-10 / STAT3 / PD-L1 signaling pathways

Deng, Xinxin; Jiao, Yanna; Hao, Huifeng; Xue, Dong; Bai, Changcai; Han, Shuyu

doi:10.1016/j.jep.2021.113978

Cited by 44 publications

(29 citation statements)

References 37 publications

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“…Several studies have shown that IFN-γ can induce PD-L1 expression through the IFN-γ/JAK/STAT1 signaling pathway, thereby promoting the immune escape of cancer cells [ 101 , 102 ]. In addition to IFN-γ, several other inflammatory cytokines also enhance PD-L1 expression on cancer cells or tumor-associated stromal cells, such as IFN-α/β [ 66 ], Toll-like receptors3/4 [ 63 , 73 ], TNF-α [ 103 ], TGF-β [ 104 ], and IL-4/6/10/17/27 [ 64 , 65 , 71 , 72 , 105 ]. Interestingly, the detection of the expression of inflammatory cytokines (e.g., IFN-γ, TNF-α, and several ILs) is a predictor of immune checkpoint therapy outcome for advanced NSCLC, while high expression of inflammatory cytokines is positively correlated with anti-PD-1 therapeutic effectiveness [ 106 ].…”

Section: The Role Of Pd-l1 In Tumor Immune Escapementioning

confidence: 99%

Extracellular vesicle PD-L1 in reshaping tumor immune microenvironment: biological function and potential therapy strategies

et al. 2022

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Programmed cell death 1 ligand 1 (PD-L1) is the ligand for programmed death protein-1 (PD-1), is associated with immunosuppression. Signaling via PD-1/PD-L1 will transmits negative regulatory signals to T cells, inducing T-cell inhibition, reducing CD8+ T-cell proliferation, or promoting T-cell apoptosis, which effectively reduces the immune response and leads to large-scale tumor growth. Accordingly, many antibody preparations targeting PD-1 or PD-L1 have been designed to block the binding of these two proteins and restore T-cell proliferation and cytotoxicity of T cells. However, these drugs are ineffective in clinical practice. Recently, numerous of studies have shown that, in addition to the surface of tumor cells, PD-L1 is also found on the surface of extracellular vesicles secreted by these cells. Extracellular vesicle PD-L1 can also interact with PD-1 on the surface of T cells, leading to immunosuppression, and has been proposed as a potential mechanism underlying PD-1/PD-L1-targeted drug resistance. Therefore, it is important to explore the production, regulation and tumor immunosuppression of PD-L1 on the surface of tumor cells and extracellular vesicles, as well as the potential clinical application of extracellular vesicle PD-L1 as tumor biomarkers and therapeutic targets.

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Section: The Role Of Pd-l1 In Tumor Immune Escapementioning

confidence: 99%

Extracellular vesicle PD-L1 in reshaping tumor immune microenvironment: biological function and potential therapy strategies

et al. 2022

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“…In the absence of IL-6, expression of PD-L1 is enhanced and the anti-PD-L1 antibody’s inhibitory activity in vivo is more significant ( 76 – 79 ). IL-18 is a pleiotropic cytokine member of the IL-1 family which has pro-inflammatory and anti-inflammatory functions ( 77 , 80 ). It is produced by a variety of cell types including macrophages.…”

Section: Tumor Immunosuppression and Immune Escapementioning

confidence: 99%

Tumor-Associated Macrophages: Key Players in Triple-Negative Breast Cancer

et al. 2022

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Triple negative breast cancer (TNBC) refers to the subtype of breast cancer which is negative for ER, PR, and HER-2 receptors. Tumor-associated macrophages (TAMs) refer to the leukocyte infiltrating tumor, derived from circulating blood mononuclear cells and differentiating into macrophages after exuding tissues. TAMs are divided into typical activated M1 subtype and alternately activated M2 subtype, which have different expressions of receptors, cytokines and chemokines. M1 is characterized by expressing a large amount of inducible nitric oxide synthase and TNF-α, and exert anti-tumor activity by promoting pro-inflammatory and immune responses. M2 usually expresses Arginase 1 and high levels of cytokines, growth factors and proteases to support their carcinogenic function. Recent studies demonstrate that TAMs participate in the process of TNBC from occurrence to metastasis, and might serve as potential biomarkers for prognosis prediction.

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“…TAMs play a substantial role in modulating the interactions between cancer cells and the immune system. In this regard, the TAM microenvironment promoted the growth of triplenegative breast cancer cells in a study by Deng et al (2021). The authors described that TAMs promoted the growth of MDA-MB-231 and MDA-MB-468 cells by upregulating the IL-10/STAT3/PD-L1 immunosuppressive signaling pathway [34].…”

Section: Cancer Promotionmentioning

confidence: 99%

“…In this regard, the TAM microenvironment promoted the growth of triplenegative breast cancer cells in a study by Deng et al (2021). The authors described that TAMs promoted the growth of MDA-MB-231 and MDA-MB-468 cells by upregulating the IL-10/STAT3/PD-L1 immunosuppressive signaling pathway [34]. revealed that TAMs might trigger PD-L1 expression by producing IFN-γ via the JAK/STAT3 and PI3K/AKT signaling cascades in A549 cells [35].…”

Section: Cancer Promotionmentioning

confidence: 99%

Flavonoids against non-physiologic inflammation attributed to cancer initiation, development, and progression—3PM pathways

et al. 2021

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Inflammation is an essential pillar of the immune defense. On the other hand, chronic inflammation is considered a hallmark of cancer initiation and progression. Chronic inflammation demonstrates a potential to induce complex changes at molecular, cellular, and organ levels including but not restricted to the stagnation and impairment of healing processes, uncontrolled production of aggressive ROS/RNS, triggered DNA mutations and damage, compromised efficacy of the DNA repair machinery, significantly upregulated cytokine/chemokine release and associated patho-physiologic protein synthesis, activated signaling pathways involved in carcinogenesis and tumor progression, abnormal tissue remodeling, and created pre-metastatic niches, among others. The anti-inflammatory activities of flavonoids demonstrate clinically relevant potential as preventive and therapeutic agents to improve individual outcomes in diseases linked to the low-grade systemic and chronic inflammation, including cancers. To this end, flavonoids are potent modulators of pro-inflammatory gene expression being, therefore, of great interest as agents selectively suppressing molecular targets within pro-inflammatory pathways. This paper provides in-depth analysis of anti-inflammatory properties of flavonoids, highlights corresponding mechanisms and targeted molecular pathways, and proposes potential treatment models for multi-level cancer prevention in the framework of predictive, preventive, and personalized medicine (PPPM / 3PM). To this end, individualized profiling and patient stratification are essential for implementing targeted anti-inflammatory approaches. Most prominent examples are presented for the proposed application of flavonoid-conducted anti-inflammatory treatments in overall cancer management.

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Taraxacum mongolicum extract inhibited malignant phenotype of triple-negative breast cancer cells in tumor-associated macrophages microenvironment through suppressing IL-10 / STAT3 / PD-L1 signaling pathways

Cited by 44 publications

References 37 publications

Extracellular vesicle PD-L1 in reshaping tumor immune microenvironment: biological function and potential therapy strategies

Extracellular vesicle PD-L1 in reshaping tumor immune microenvironment: biological function and potential therapy strategies

Tumor-Associated Macrophages: Key Players in Triple-Negative Breast Cancer

Flavonoids against non-physiologic inflammation attributed to cancer initiation, development, and progression—3PM pathways

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