IL‐1β from M2 macrophages promotes migration and invasion of ESCC cells enhancing epithelial‐mesenchymal transition and activating NF‐κB signaling pathway

Zhou, Jian; Zheng, Shu; Liu, Tao; Liu, Qing; Chen, Yumei; Tan, Doudou; Ma, Rong; Lü, Xiaomei

doi:10.1002/jcb.26918

Cited by 36 publications

(28 citation statements)

References 32 publications

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“…It has been previously suggested that EMT could be associated with a pro-tumorigenic microenvironment in lung cancer 41 . In esophageal squamous cell carcinoma, M2 macrophages promote migration, invasion, and enhance EMT 42 . On the other hand, mast cells have been associated with angiogenesis in breast cancer 43 .…”

Section: Discussionmentioning

confidence: 99%

An independent poor-prognosis subtype of breast cancer defined by a distinct tumor immune microenvironment

et al. 2019

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How mixtures of immune cells associate with cancer cell phenotype and affect pathogenesis is still unclear. In 15 breast cancer gene expression datasets, we invariably identify three clusters of patients with gradual levels of immune infiltration. The intermediate immune infiltration cluster (Cluster B) is associated with a worse prognosis independently of known clinicopathological features. Furthermore, immune clusters are associated with response to neoadjuvant chemotherapy. In silico dissection of the immune contexture of the clusters identified Cluster A as immune cold, Cluster C as immune hot while Cluster B has a pro-tumorigenic immune infiltration. Through phenotypical analysis, we find epithelial mesenchymal transition and proliferation associated with the immune clusters and mutually exclusive in breast cancers. Here, we describe immune clusters which improve the prognostic accuracy of immune contexture in breast cancer. Our discovery of a novel independent prognostic factor in breast cancer highlights a correlation between tumor phenotype and immune contexture.

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Section: Discussionmentioning

confidence: 99%

An independent poor-prognosis subtype of breast cancer defined by a distinct tumor immune microenvironment

et al. 2019

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“…Chen et al reported that IL-1β was expressed in human ESCC cell [ 47 ]. IL-1β was also expressed in M2 TAMs in human ESCC [ 13 , 48 ]. We suggest that IL-1β derived from ESCC cells and/or TAMs may induce CCL3 secretion from TAMs; however the role of IL-1β against TAMs in ESCC was not well understood.…”

Section: Discussionmentioning

confidence: 99%

CCL3–CCR5 axis contributes to progression of esophageal squamous cell carcinoma by promoting cell migration and invasion via Akt and ERK pathways

Kodama

Koma

Arai

et al. 2020

Laboratory Investigation

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Tumor-associated macrophages (TAMs) contribute to the progression and mortality of various malignancies. We reported that high numbers of infiltrating TAMs were significantly associated with tumor progression and poor prognosis in esophageal squamous cell carcinoma (ESCC). In our previous investigation of TAMs’ actions in ESCC, we compared gene expression profiles between peripheral blood monocyte (PBMo)-derived macrophages and TAM-like macrophages stimulated with conditioned media of ESCC cell lines. Among the upregulated genes in the TAM-like macrophages, we focused on CC chemokine ligand 3 ( CCL3 ), which was reported to contribute to tumor progression in several malignancies. Herein, we observed that not only TAMs but also ESCC cell lines expressed CCL3. A CCL3 receptor, CC chemokine receptor 5 (CCR5) was expressed in the ESCC cell lines. Treating the ESCC cell lines with recombinant human (rh)CCL3 induced the phosphorylations of Akt and ERK, which were suppressed by CCR5 knockdown. Migration and invasion of ESCC cells were promoted by treatment with rhCCL3 and co-culture with TAMs. TAMs/rhCCL3-promoted cell migration and invasion were suppressed by inhibition of the CCL3–CCR5 axis, PI3K/Akt, and MEK/ERK pathways. Treatment with rhCCL3 upregulated MMP2 and VEGFA expressions in ESCC cell lines. Our immunohistochemical analysis of 68 resected ESCC cases showed that high expression of CCL3 and/or CCR5 in ESCC tissues was associated with poor prognosis. High CCR5 expression was associated with deeper invasion, presence of vascular invasion, higher pathological stage, higher numbers of infiltrating CD204 + TAMs, and higher microvascular density. High expression of both CCL3 and CCR5 was an independent prognostic factor for disease-free survival. These results suggest that CCL3 derived from both TAMs and cancer cells contributes to the progression and poor prognosis of ESCC by promoting cell migration and invasion via the binding of CCR5 and the phosphorylations of Akt and ERK. The CCL3–CCR5 axis could become the target of new therapies against ESCC.

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“…M2 macrophages are regarded as tumor-promotive and are correlated with poor prognosis in various cancers, including ESCC (43,44). M2 macrophages could promote tumor metastasis by inducing epithelial-mesenchymal transition (EMT) or secreting cytokines such as IL-1β (45). The infiltrated immune cell can induce the host immune response to inhibit or promote the progression of tumor cells in the tumor microenvironment (42).…”

Section: Discussionmentioning

confidence: 99%

The Prognostic Significance of Metabolic Syndrome and a Related Six-lncRNA Signature in Esophageal Squamous Cell Carcinoma

et al. 2020

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Background: Metabolic syndrome (MetS) is associated with the development of esophageal squamous cell carcinoma (ESCC), and long non-coding RNAs (lncRNAs) are involved in a variety of mechanisms of MetS and tumor. This study will explore the prognostic effect of MetS and the associated lncRNA signature on ESCC.Methods: Our previous RNA-chip data (GSE53624, GSE53622) for 179 ESCC patients were reanalyzed according to MetS. The recurrence-free survival (RFS) was collected for these patients. The status of the MetS-related tumor microenvironment was analyzed with the CIBERSORT and ESTIMATE algorithms. A lncRNA signature was established with univariate and multivariate Cox proportional hazards regression (PHR) analysis and verified using the Kaplan-Meier survival curve analysis and time-dependent receiver operating characteristic (ROC) curves. A clinical predictive model was constructed based on multiple risk factors, evaluated using C-indexes and calibration curves, and verified using data from the GEO and TCGA databases. Results:The results showed that MetS was an independent risk factor for ESCC patients conferring low OS and RFS. Tumor microenvironment analysis indicated that patients with MetS have high stromal scores and M2 macrophage infiltration. A six-lncRNA signature was established by 60 ESCC patients randomly selected from GSE53624 and identified with an effective predictive ability in validation cohorts (59 patients from GSE53624 and 60 patients from GSE53622), subgroup analysis, and ESCC patients from TCGA. MetS and the six-lncRNA signature could be regarded as independent risk factors and enhanced predictive ability in the clinical predictive model. Conclusions:Our results indicated that MetS was associated with poor prognosis in ESCC patients, and the possible mechanism was related to changes in the tumor microenvironment. MetS and the six-lncRNA signature could also serve as independent risk factors with available clinical application value.

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IL‐1β from M2 macrophages promotes migration and invasion of ESCC cells enhancing epithelial‐mesenchymal transition and activating NF‐κB signaling pathway

Cited by 36 publications

References 32 publications

An independent poor-prognosis subtype of breast cancer defined by a distinct tumor immune microenvironment

An independent poor-prognosis subtype of breast cancer defined by a distinct tumor immune microenvironment

CCL3–CCR5 axis contributes to progression of esophageal squamous cell carcinoma by promoting cell migration and invasion via Akt and ERK pathways

The Prognostic Significance of Metabolic Syndrome and a Related Six-lncRNA Signature in Esophageal Squamous Cell Carcinoma

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