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Cyr61 promotes CD204 expression and migration of macrophages via MEK/Erk pathway in the microenvironment of human esophageal squamous cell carcinoma

ABSTRACT: The authors previously suggested that CD204 was a useful marker for tumor-associated macrophages (TAMs) of esophageal squamous cell carcinoma (ESCC). In this study, they discovered that within ESCC microenvironment not only cancer cells but also TAMs expressed cysteine-rich, angiogenic inducer, 61 (Cyr61), induced by conditioned media of ESCC cells. Levels of Cyr61 expression were associated with CD204+ macrophage infiltration in ESCC tissue. Cyr61 promoted CD204 expression and migration of macrophages via MEK/Erk pathway in vitro.

ORGANISM(S): Homo sapiens

PROVIDER: GSE59471 | GEO | 2014/10/08

SECONDARY ACCESSION(S): PRJNA255400

REPOSITORIES: GEO

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Cyr61 promotes CD204 expression and migration of macrophages via MEK/Erk pathway in the microenvironment of human esophageal squamous cell carcinoma

Project description:The authors previously suggested that CD204 was a useful marker for tumor-associated macrophages (TAMs) of esophageal squamous cell carcinoma (ESCC). In this study, they discovered that within ESCC microenvironment not only cancer cells but also TAMs expressed cysteine-rich, angiogenic inducer, 61 (Cyr61), induced by conditioned media of ESCC cells. Levels of Cyr61 expression were associated with CD204+ macrophage infiltration in ESCC tissue. Cyr61 promoted CD204 expression and migration of macrophages via MEK/Erk pathway in vitro. To identify the molecules specifically upregulated in TAM-like THP-1 cells, we performed a cDNA microarray analysis using RNAs from THP-1 stimulated with 200 nM TPA or with 200 nM TPA followed by 50% TE-8CM. THP-1 human acute monocytic leukemia cell line was treated with 200 nM 12-O-tetradecanoylphorbol-13-acetate (TPA) for 2 days to induce macrophage-like differentiation, then exposed to 50%Conditioned medium of TE-8 ESCC cell line (TE-8CM) for 2 days. Differentially expressed genes between MM-NM-&-like and TAM-like THP-1 cells were analysed by cDNA microarray. TE-8CM was prepared by plating 5 M-CM-^W 106 tumor cells in 10 mL complete medium in 100-mm dishes for 24 hr, thereafter changing the medium to complete DMEM supplemented with 10% human AB serum instead of fetal bovine serum. After 2M-bM-^@M-^S3 days, the supernatants were harvested, centrifuged and stored in aliquots at M-bM-^HM-^R80M-BM-0C.

2014-10-08 | E-GEOD-59471 | biostudies-arrayexpress

CYR61 orchestrates NASH fibrosis through SYK-NFκB-PDGF signaling in monocyte-derived macrophages [bulk RNA-seq]

Project description:Obesity is increasing worldwide and leads to a multitude of metabolic diseases including non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatosis (NASH). Here we examine the role of CYR61 in liver fibrosis and inflammation and its potential as a therapeutic target. Loss of CYR61 during NASH injury improves glucose tolerance, decreases liver inflammation and reduces fibrosis. CYR61 activates signaling in monocytes and monocyte-derived macrophages promoting a pro-inflammatory/pro-fibrotic phenotype through a CYR61/SYK/NFKB signaling cascade. In vitro, CYR61 activates Pdgfa and Pdgfb expression in macrophages in a NFκB-dependent manner. Ultimately, we identify a potential therapeutic for NASH: a CYR61-blocking antibody that reduces fibrotic injury and CYR61-driven signaling in macrophages in vitro and in vivo. This study demonstrates that CYR61 is a key driver of liver inflammation and fibrosis and a strong therapeutic target for treatment of NAFLD/NASH.

2023-10-02 | GSE199637 | GEO

CYR61 orchestrates NASH fibrosis through SYK-NFκB-PDGF signaling in monocyte-derived macrophages [HIVE single-cell RNA-seq]

2023-10-02 | GSE199639 | GEO

CYR61 orchestrates NASH fibrosis through SYK-NFκB-PDGF signaling in monocyte-derived macrophages [10X single-cell RNA-seq]

2023-10-02 | GSE199638 | GEO

RNA-seq of CYR61-treated murine bone marrow-derived macrophages

Project description:We assess the effect of CYR61 treatment on the transcriptome of mouse bone marrow-derived macrophages.

2023-10-18 | GSE222100 | GEO

GDF15 overexpression dreived from tumor-associated macrophages and cancer cells in the microenvironment of human esophageal squamous cell carcinoma promotes tumor growth and poor prognosis

Project description:Tumor-associated macrophages (TAMs) are known to be involved in progression, angiogenesis and motility of various cancers. We have previously reported the association between increased number of infiltrating TAMs with tumor progression and poor prognosis in esophageal squamous cell carcinomas (ESCCs). To study roles of TAMs in ESCC, we first exposed peripheral blood monocytes (PBMo) derived macrophages from healthy volunteers to conditioned media of TE series human ESCC cell line (TECM) and confirmed the induction of expression of M2 macrophage marker, CD204, and protumorigenic factors, interleukin (IL)-10, VEGFA and MMPs. Next, we compared gene expression profile between PBMo-derived macrophages and PBMo-derived macrophages stimulated with TECM by cDNA microarray. Based on the result, we focused on growth differentiation factor 15 (GDF15) among highly expressed genes including IL-6, IL-8 and CXCL1. Immunohistochemical study on 70 cases of surgically resected ESCCs revealed that GDF15 was detected not only in macrophages but also in cancer cells. High expression of GDF15 in ESCCs was significantly correlated with more malignant phenotypes including lymph and blood vessel invasion, lymph node metastasis as well as clinical stages. Patients with high expression of GDF15 showed poor disease-free survival (p = 0.011) and overall survival (p = 0.041). Furthermore, we found that recombinant human GDF15 promote cell proliferation and phosphorylation of both Akt and Erk1/2 in ESCC cell lines in vitro. These results indicate that GDF15 is secreted by both TAMs and cancer cells in tumor microenvironment and is associated with aberrant growth and poor prognosis of human ESCC. We exposed PBMo-derived macrophages from healthy volunteers to TECM and observed their acquisition of TAM-like characters in this study. We further investigated specific cancer-associated gene expression profile in TECM induced TAM-like macrophages by cDNA microarray analysis.

2014-08-01 | E-GEOD-59948 | biostudies-arrayexpress

Bulk RNA-seq of: HUVECs co-incubated with CYR61-treated mouse bone marrow-derived macrophages CYR61-treated murine bone marrow-derived macrophages CYR61-treated HUVECs and CYR61-treated human THP1 monocytes

Project description:Bulk RNA-seq of: HUVECs co-incubated with CYR61-treated mouse bone marrow-derived macrophages CYR61-treated murine bone marrow-derived macrophages CYR61-treated HUVECs and CYR61-treated human THP1 monocytes

| PRJNA917714 | ENA

SPP1 represents a therapeutic target that promotes the progression of esophageal squamous cell carcinoma by driving M2 macrophage infiltration

Project description:Background: Tumor-associated macrophages (TAMs) are an important component of the tumor microenvironment (TME). However, the crosstalk between esophageal squamous cell carcinoma (ESCC) cells and TAMs remains largely unexplored. Methods: Clinical samples and the TCGA database were used to evaluate the relevance of SPP1 and TAM infiltration in ESCC. Mouse models were constructed to investigate the roles of macrophages educated by SPP1 in ESCC. Macrophage phenotypes were determined using qRT‒PCR and immunohistochemical staining. RNA sequencing was performed to elucidate the mechanism. Results: Increasing expression of SPP1 correlated with M2-like TAM accumulation in ESCC, and they both predicted poor prognosis in the ESCC cohort. Knockdown of SPP1 significantly inhibited the infiltration of M2 TAMs in xenograft tumors. In vivo mouse model experiments showed that SPP1-mediated education of macrophages plays essential roles in the progression of ESCC. Mechanistically, SPP1 recruited macrophages and promoted M2 polarization via CD44/PI3K/AKT signaling activation and then induced VEGFA and IL6 secretion to sustain ESCC progression. Finally, blockade of SPP1 with RNA aptamer significantly inhibited tumor growth and M2 TAM infiltration in xenograft mouse models. Conclusions: This study highlights a SPP1-mediated crosstalk between ESCC cells and TAMs in ESCC. SPP1 could serve as a potential target in ESCC therapy.

2024-09-09 | GSE256360 | GEO

ANXA10 induction by interaction with tumor-associated macrophages promotes the growth of esophageal squamous cell carcinoma

Project description:Tumor-associated macrophages (TAMs) have important roles in the progression, angiogenesis and motility of various cancers. To study the effects of TAMs on the tumor microenvironment of ESCCs, we constructed an in vitro system for the differentiation of peripheral blood monocyte (PBMo)-derived macrophages into TAM-like PBMo-derived macrophages. We established a co-culture assay using a human ESCC cell line and TAM-like PBMo-derived macrophages and we performed a cDNA microarray analysis between monocultured and co-cultured ESCC cell lines. Our qRT-PCR confirmed that in the co-cultured ESCC cell lines, CYP1A1, DHRS3, ANXA10, KLK6 and CYP1B1 mRNA were highly up-regulated; AMTN and IGFL1 mRNA were down-regulated. We observed that a high ANXA10 expression was closely associated with the depth of invasion and high numbers of infiltrating CD68+ and CD204+ TAMs. ESCC patients with high ANXA10 expression were significantly correlated with poor disease-free survival (p = 0.0216). ANXA10 knockdown using siRNA significantly suppressed the cell growth of TE-8 and TE-9 ESCC cells by inhibiting Akt and Erk1/2 signaling pathways. We confirmed that ANXA10 overexpression induced the cell growth of TE-15 ESCC cells by activating Akt and Erk1/2 phosphorylation. These results suggest that ANXA10 induced by TAMs in the tumor microenvironment is associated with aberrant growth and a poor prognosis in human ESCC tissues.

2018-08-17 | GSE118642 | GEO

Tetracycline-Inducible Cyr61 effect on LN229 glioma cells

Project description:Glioblastoma multiforme is the most common and aggressive form of brain cancer. The use of oncolytic HSV-1 (oHSV) to selectively target brain cancer cells leading to their lytic destruction has shown to be very promising in a preclinical setting, but is lacking efficacy in clinical trials. Cyr61, a secreted extracellular matrix protein which functions to promote angiogenesis, migration, proliferation and tumorigenesis, was found to be upregulated rapidly following oHSV infection. Here we show, using microarray analysis, that Cyr61 expression leads to the induction of several genes with type 1 interferon function. We show that Cyr61 mediated type 1 IFN induction is through its interaction with integrin alpha6beta1 on the cell surface and results in oHSV inhibition, reducing the efficacy of this therapy. We used microarray to detail the global program of gene expression underlying Cyr61 mediated oncolytic HSV-1 inhibition and identified distinct classes of up-regulated genes during this process. Tetracycline-Inducible glioma cells expressing Cyr61 protein in the presence of doxycycline were treated with or without doxycycline for 24 hours. RNA was extracted and hybridized on Affymetrix microarray. Two groups: Â± dox to induce cyr61, performed in triplicate.

2012-04-03 | E-GEOD-29384 | biostudies-arrayexpress

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