Bu Fei Decoction attenuates the tumor associated macrophage stimulated proliferation, migration, invasion and immunosuppression of non-small cell lung cancer, partially via IL-10 and PD-L1 regulation

Pang, Lei; Han, Shuyu; Jiao, Yanna; Jiang, Shantong; He, Xiran; Li, Pingping

doi:10.3892/ijo.2017.4014

Cited by 57 publications

(63 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Upon on those findings, we hypothesize that autocrine VEGF operation by transient activation of monocytes/macrophages highly depends on the soluble factors, including IFN‐γ, IL‐10 and the proportion of proinflammatory cytokines in the milieu. In combination with our finding and the evidence demonstrated that elevated PD‐L1 expression on TAM can be inhibited by anti‐IL‐10 antibody, therefore, the PD‐L1 expression on TAM regulated by autocrine VEGF potentially existed.…”

Section: Discussionsupporting

confidence: 86%

See 1 more Smart Citation

Autocrine VEGF signalling on M2 macrophages regulates PD‐L1 expression for immunomodulation of T cells

Lai

Wahyuningtyas

Aui

et al. 2018

J Cellular Molecular Medi

View full text Add to dashboard Cite

M2‐polarized macrophages, on one hand, can promote tumour vascularization by producing proangiogenic factors, such as vascular endothelial growth factor (VEGF). On the other hand, the expression of VEGF receptors (VEGFR) in this cell lineage was also reported. Although the function of VEGF/VEGFR axis plays a pivotal role in macrophages infiltration and angiogenesis, however, there is still lack of the direct evidence to show the role of VEGF as an autocrine operating in M2 macrophages, particularly for immunomodulation. In our study, we surprisingly discovered that M2 macrophages polarized by baicalin can simultaneously express VEGF and its receptors. Taking advantage of this unique culture system, we were able to investigate the biological activity of M2 macrophages in response to the autocrine VEGF milieu. Our results showed that the expression of programmed death‐ligand 1 (PD‐L1) on M2 macrophages was significantly up‐regulated in autocrine VEGF milieu. Through the blockade of autocrine VEGF signalling, PD‐L1 expression on M2 macrophages was dramatically down‐regulated. Furthermore, transplantation of PD‐L1+ M2 macrophage stimulated by autocrine VEGF into allogeneic mice significantly suppressed host CD4+/CD8+ T cells in the peripheral blood and increased CD4+ CD25+ regulatory T cells in the bone marrow. In conclusion, our findings provide a novel biological basis to support the current successful strategy using combined VEGF/PD‐1 signalling blockade in cancer therapy.

show abstract

Section: Discussionsupporting

confidence: 86%

“…In combination with our finding and the evidence demonstrated that elevated PD-L1 expression on TAM can be inhibited by anti-IL-10 antibody, 34 therefore, the PD-L1 expression on TAM regulated by autocrine VEGF potentially existed.…”

Section: Corelation Of M2 Macrophages and Vegfsupporting

confidence: 87%

Autocrine VEGF signalling on M2 macrophages regulates PD‐L1 expression for immunomodulation of T cells

Lai

Wahyuningtyas

Aui

et al. 2018

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…Tumor-associated macrophages (TAMs) are one of the most abundant immune cell populations in the TME [25][26][27]. TAMs might be a potential marker for poor prognosis.…”

Section: Discussionmentioning

confidence: 99%

Identification of key genes related to macrophage infiltration in gastric cancer based on WGCNA

Chen¹,

Zhang

Cao

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Gastric cancer (GC) is rampant around the world. Most of the GC cases are detected in advanced stages with poor prognosis. The identification of marker genes for early diagnosis is of great significance. Studying the tumor environment is helpful to acknowledge the process of tumorigenesis, development, and metastasis.Methods: In GEO, 22 kinds of immune cell infiltration were calculated by CIBERSORT. Macrophages were discovered remarkably infiltrated higher in GC compared with normal tissues. WGCNA was utilized to construct the network and then identify key modules and genes related to macrophages in TCGA.Results: Finally, 18 hub genes were verified. In the PPI bar chart, the top 3 genes were chosen as hub genes involved in most pathways. On the TIMER and THPA websites, it is verified that the expression levels of CYBB, CD86 and C3AR1 genes in tumor tissues were higher than those in normal tissues.Conclusion: These genes may work as biomarkers or targets for accurate diagnosis and treatment of GC in the future. Our findings may be a new strategy for the treatment of GC.

show abstract

“…Tumour associated macrophages (TAMs) derived from monocytes in the blood are recruited by cytokines and chemokines secreted by cancer cells to constitute a crucial element of tumour stromal cells . TAMs provide immune escape for cancer cells by expressing immunosuppressive cytokines (IL‐10) which induces T cell dysfunction and promote tumour invasion and migration by secreting extracellular matrix remodeling enzymes (MMP‐1, MMP‐3, MMP‐10) . Under the action of colony‐stimulating factor (CSF), TAMs contribute to the enhanced invasion, angiogenesis, and immunoregulation of non‐small cell lung cancer .…”

Section: Involvement Of Microenvironmental Factors In Cca Occvurrencementioning

confidence: 99%

The role of tumour microenvironment: a new vision for cholangiocarcinoma

Chen

Guo

Xie

et al. 2018

J Cellular Molecular Medi

View full text Add to dashboard Cite

Cholangiocarcinoma (CCA) is a relatively rare malignant and lethal tumour derived from bile duct epithelium and the morbidity is now increasing worldwide. This disease is difficult to diagnose at its inchoate stage and has poor prognosis. Therefore, a clear understanding of pathogenesis and major influencing factors is the key to develop effective therapeutic methods for CCA. In previous studies, canonical correlation analysis has demonstrated that tumour microenvironment plays an intricate role in the progression of various types of cancers including CCA. CCA tumour microenvironment is a dynamic environment consisting of authoritative tumour stromal cells and extracellular matrix where tumour stromal cells and cancer cells can thrive. CCA stromal cells include immune and non‐immune cells, such as inflammatory cells, endothelial cells, fibroblasts, and macrophages. Likewise, CCA tumour microenvironment contains abundant proliferative factors and can significantly impact the behaviour of cancer cells. Through abominably intricate interactions with CCA cells, CCA tumour microenvironment plays an important role in promoting tumour proliferation, accelerating neovascularization, facilitating tumour invasion, and preventing tumour cells from organismal immune reactions and apoptosis. This review summarizes the recent research progress regarding the connection between tumour behaviours and tumour stromal cells in CCA, as well as the mechanism underlying the effect of tumour stromal cells on the growth of CCA. A thorough understanding of the relationship between CCA and tumour stromal cells can shed some light on the development of new therapeutic methods for treating CCA.

show abstract

Bu Fei Decoction attenuates the tumor associated macrophage stimulated proliferation, migration, invasion and immunosuppression of non-small cell lung cancer, partially via IL-10 and PD-L1 regulation

Cited by 57 publications

References 46 publications

Autocrine VEGF signalling on M2 macrophages regulates PD‐L1 expression for immunomodulation of T cells

Autocrine VEGF signalling on M2 macrophages regulates PD‐L1 expression for immunomodulation of T cells

Identification of key genes related to macrophage infiltration in gastric cancer based on WGCNA

The role of tumour microenvironment: a new vision for cholangiocarcinoma

Contact Info

Product

Resources

About