Tumor-associated macrophages promote migration and invasion via modulating IL-6/STAT3 signaling in renal cell carcinoma

Chen, Heng; Qian, Subo; Zhang, Lin; Pan, Xiuwu; Qu, Fajun; Yu, Yongjiang; Gu, Zhengqin; Cui, Xingang; Shen, Haibo

doi:10.1016/j.intimp.2022.109139

Cited by 11 publications

(8 citation statements)

References 35 publications

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“…In our previous study, we investigated the infiltration and functions of TAMs in RCC. We observed a significant increase in TAM infiltration in RCC, suggesting their potential role in promoting RCC progression by regulating IL‐6/STAT3 signaling 15 . A published study reported that FOXK1 promotes the recruitment of TAMs by regulating CCL2 expression 19 .…”

Section: Discussionmentioning

confidence: 54%

“…IHC was carried out with tissue slides as previous described 15 . Briefly, the tissue sections underwent antigen retrieval, were blocked with goat serum, and incubated with the primary antibody against FOXK1 (Immunoway) overnight at 4°C.…”

Section: Methodsmentioning

confidence: 99%

“…IHC was carried out with tissue slides as previous described. 15 Briefly, the tissue sections underwent antigen retrieval, were blocked with goat serum, and incubated with the primary antibody against FOXK1 (Immunoway) overnight at 4°C. The sections were then incubated with HRP-conjugated secondary antibody (Servicebio) at room temperature for 2 h. Subsequently, the sections were stained with diaminobenzidine (DAB)-H 2 O 2 and hematoxylin.…”

Section: Immunohistochemistry (Ihc)mentioning

confidence: 99%

“…We previously demonstrated that the infiltration of TAMs was increased in RCC tumor tissues and TAMs may contribute to RCC progression. 15 Another published study reported that FOXK1 regulates the recruitment of TAMs by controlling CCL2 expression. 19 In our study, we examined the expressions of CCL2 and TAM markers CD163 and CD206 in RCC tumor tissues.…”

Section: Foxk1 Upregulation Is Associated With Tams Infiltration In Rccmentioning

confidence: 99%

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FOXK1 upregulation is correlated with tumor progression and tumor associated macrophages infiltration in renal cell carcinoma

Chen,

Pan,

Zhang

et al. 2023

Molecular Carcinogenesis

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Renal cell carcinoma (RCC) is one of the most common urological cancers in adults. Forkhead box k1 (FOXK1) is a transcription factor involved in the progression of various malignant tumors. In this study, we aimed to investigate the expression and roles of FOXK1 in RCC development. Our findings revealed increased expression of FOXK1 in RCC tumor tissues and cell lines compared with normal controls. Functional assays demonstrated that knockdown of FOXK1 significantly inhibited proliferation, migration, invasion, and promoted apoptosis in RCC cells. Furthermore, FOXK1 knockdown suppressed epithelial‐mesenchymal transition and Wnt signaling in RCC cells. Additionally, we observed a correlation between FOXK1 upregulation and tumor associated macrophages infiltration in RCC. These results suggest that FOXK1 acts as an oncogene in RCC and may serve as a potential therapeutic target for RCC treatment.

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Section: Discussionmentioning

confidence: 54%

Section: Methodsmentioning

confidence: 99%

Section: Immunohistochemistry (Ihc)mentioning

confidence: 99%

Section: Foxk1 Upregulation Is Associated With Tams Infiltration In Rccmentioning

confidence: 99%

See 2 more Smart Citations

FOXK1 upregulation is correlated with tumor progression and tumor associated macrophages infiltration in renal cell carcinoma

Chen,

Pan,

Zhang

et al. 2023

Molecular Carcinogenesis

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“…In inflammatory TME, IL-6 secreted by TAMs resulting in a vicious cycle that further promote macrophages polarization to TAMS and increase IL-6 expression which can lead to a smoldering inflammatory state, and enhance tumor cell metastasis ( 46 , 59 ). Chen S,et al showed that IL-6 was responsible for TAMs induced renal cell carcinoma cells migration, invasion, EMT by activating I L-6/STAT3 signaling ( 60 ). IL-6 acts on IL-6R/gp130 receptors and active STAT3 signaling which can promote epithelial-mesenchymal transition (EMT), angiogenesis and immunosuppression in cancers ( 61 ).…”

Section: Factors Affecting the Polarization Of Tumor Macrophages In Tmementioning

confidence: 99%

Tumor−associated macrophage polarization in the inflammatory tumor microenvironment

Zou

Lin

et al. 2023

Front. Oncol.

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The chronic inflammation of tumor continues to recruit TAMs (tumor−associated macrophages) to the TME (tumor microenvironment) and promote polarization. Pro-inflammatory signals polarize macrophages to the M1 phenotype to enhance inflammation against pathogens. Tumor inflammatory development changes the pro-inflammatory response to an anti-inflammatory response, resulting in the alteration of macrophages from M1 to M2 to promote tumor progression. Additionally, hypoxia activates HIF (hypoxia-inducible factors) in the TME, which reprograms macrophages to the M2 phenotype to support tumor development. Here, we discuss the factors that drive phenotypic changes in TAMs in the inflammatory TME, which will help in the development of cancer immunotherapy of macrophages.

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Crosstalk between cancer cells and macrophages promotes OSCC cell migration and invasion through a CXCL1/EGF positive feedback loop

Huang,

Jiang,

Lin

et al. 2024

Discov Onc

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Background C-X-C motif chemokine ligand 1 (CXCL1) and epithelial growth factor (EGF) are highly secreted by oral squamous cell carcinoma (OSCC) cells and tumor-associated macrophages, respectively. Recent studies have shown that there is intricate "cross-talk" between OSCC cells and macrophages. However, the underlying mechanisms are still poorly elucidated. Methods The expression of CXCL1 was detected by immunohistochemistry in OSCC clinical samples. CXCL1 levels were evaluated by RT‒PCR and ELISA in an OSCC cell line and a normal epithelial cell line. The expression of EGF was determined by RT‒PCR and ELISA. The effect of EGF on the proliferation of OSCC cells was evaluated by CCK-8 and colony formation assays. The effect of EGF on the migration and invasion ability and epithelial-mesenchymal transition (EMT) of OSCC cells was determined by wound healing, Transwell, RT‒PCR, Western blot and immunofluorescence assays. The polarization of macrophages was evaluated by RT‒PCR and flow cytometry. Western blotting was used to study the molecular mechanism in OSCC. Results The expression of C-X-C motif chemokine ligand 1 (CXCL1) was higher in the OSCC cell line (Cal27) than in immortalized human keratinocytes (Hacat cells). CXCL1 derived from Cal27 cells upregulates the expression of epithelial growth factor (EGF) in macrophages. Paracrine stimulation mediated by EGF further facilitates the epithelial-mesenchymal transition (EMT) of Cal27 cells and initiates the upregulation of CXCL1 in a positive feedback-manner. Mechanistically, EGF signaling-induced OSCC cell invasion and migration can be ascribed to the activation of NF-κB signaling mediated by the epithelial growth factor receptor (EGFR), as determined by western blotting. Conclusions OSCC cell-derived CXCL1 can stimulate the M2 polarization of macrophages and the secretion of EGF. Moreover, EGF significantly activates NF-κB signaling and promotes the migration and invasion of OSCC cells in a paracrine manner. A positive feedback loop between OSCC cells and macrophages was formed, contributing to the promotion of OSCC progression.

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Tumor-associated macrophages promote migration and invasion via modulating IL-6/STAT3 signaling in renal cell carcinoma

Cited by 11 publications

References 35 publications

FOXK1 upregulation is correlated with tumor progression and tumor associated macrophages infiltration in renal cell carcinoma

FOXK1 upregulation is correlated with tumor progression and tumor associated macrophages infiltration in renal cell carcinoma

Tumor−associated macrophage polarization in the inflammatory tumor microenvironment

Crosstalk between cancer cells and macrophages promotes OSCC cell migration and invasion through a CXCL1/EGF positive feedback loop

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