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il6/stat3/mir-506-3p/foxq1 signal cascade bio-rad chemidoc xrs + system jak2/stat3/mir-506-3p/foxq1 axis stat3-repressed mir-34a stat3-mediated mir-506-3p expression undergo epithelial-mesenchymal transition ck+/vimentin−/cd45−/hoechst+ cell ck−/vimentin+/cd45−/hoechst+ cell ck−/vimentin−/cd45−/hoechst+ cell stat3/mir-506-3p/foxq1 axis hrp-conjugated secondary antibodies hct116 + tams/si-control group compared predicted mir-506-3p–binding sites hct116 + tam/si-con groups stat3-mir-506-3p-foxq1 pathway stat3/mir-506-3p/foxq1 pathway promote epithelial-mesenchymal transition epithelial–mesenchymal transition phenotype stat3-based mir-506-3p regulation hct116 + tam/si-il6 groups il-6 mediates cross-talk fitc-labeled anti-ck colorectal surgical oncology mesenchymal ctc-mediated metastasis mir-506-3p promoter regions af647-labeled anti-cd45 systemic t-cell response stat3-suppressed reporter system hct116 + tams/si-il6 group exert antagonistic functions-protumor kruskal-wallis nonparametric analysis mir-506-3p-foxq1 axis mir-506-3p/foxq1 axis bin xiong article download pdf hct116 + tams/si-control group tumor suppressor mir-506-3p hct116 + tams/si-control compared hct116 + tam/si-con enzyme-linked immunosorbent assay dual-luciferase reporter system multivariate cox-regression analyses epithelial–mesenchymal transition epithelial-mesenchymal transition representative emt/inflammation related-cytokines stat3-mediated promoter regulation wedge-shaped microfluidic chip immune-microenvironment confers chemoresistance pe-labeled anti-vimentin ctc-mediated tumor metastasis

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         headline:Crosstalk between cancer cells and tumor associated macrophages is required for mesenchymal circulating tumor cell-mediated colorectal cancer metastasis
         description:Tumor-associated macrophages (TAMs) are major components of tumor microenvironment that frequently associated with tumor metastasis in human cancers. Circulating tumor cell (CTC), originating from primary tumor sites, is considered to be the precursors of tumor metastasis. However, the regulatory mechanism of TAMs in CTC-mediated tumor metastasis still remains unclear. Immunohistochemical staining was used to detect the macrophages infiltration (CD68 and CD163), epithelial–mesenchymal transition (EMT) markers (E-cadherin and Vimentin) expression in serial sections of human colorectal cancer (CRC) specimens. Then, the correlations between macrophages infiltration and clinicopathologic features, mesenchymal CTC ratio, and patients’ prognosis were analyzed. A co-culture assay in vitro was used to evaluate the role of TAMs on CRC EMT, migration and invasion, and ELISA, luciferase reporter assay and CHIP were performed to uncover the underlying mechanism. Furthermore, an in vivo model was carried out to confirm the effect of TAMs on mesenchymal CTC-mediated metastasis. Clinically, CD163+ TAMs infiltrated in invasive front was associated with EMT, mesenchymal CTC ratio, and poor prognosis in patients with CRC. CRC–conditioned macrophages regulated EMT program to enhance CRC cells migration and invasion by secreting IL6. TAMs-derived IL6 activated the JAK2/STAT3 pathway, and activated STAT3 transcriptionally inhibited the tumor suppressor miR-506-3p in CRC cells. miR-506-3p, a key miRNA regulating FoxQ1, was downregulated in CRC cells, resulting in increased FoxQ1 expression, which in turn led to the production of CCL2 that promoted macrophage recruitment. Inhibition of CCL2 or IL6 broke this loop and reduced macrophage migration and mesenchymal CTC-mediated metastasis, respectively. Our data indicates that TAMs induce EMT program to enhance CRC migration, invasion, and CTC-mediated metastasis by regulating the JAK2/STAT3/miR-506-3p/FoxQ1 axis, which in turn leads to the production of CCL2 that promote macrophage recruitment, revealing a new cross-talk between immune cells and tumor cells in CRC microenvironment.
         datePublished:2019-03-30T00:00:00Z
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            Tumor-associated macrophages
            Colorectal cancer
            EMT
            Circulating tumor cell
            Metastasis
            Prognosis
            Cancer Research
            Oncology
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      headline:Crosstalk between cancer cells and tumor associated macrophages is required for mesenchymal circulating tumor cell-mediated colorectal cancer metastasis
      description:Tumor-associated macrophages (TAMs) are major components of tumor microenvironment that frequently associated with tumor metastasis in human cancers. Circulating tumor cell (CTC), originating from primary tumor sites, is considered to be the precursors of tumor metastasis. However, the regulatory mechanism of TAMs in CTC-mediated tumor metastasis still remains unclear. Immunohistochemical staining was used to detect the macrophages infiltration (CD68 and CD163), epithelial–mesenchymal transition (EMT) markers (E-cadherin and Vimentin) expression in serial sections of human colorectal cancer (CRC) specimens. Then, the correlations between macrophages infiltration and clinicopathologic features, mesenchymal CTC ratio, and patients’ prognosis were analyzed. A co-culture assay in vitro was used to evaluate the role of TAMs on CRC EMT, migration and invasion, and ELISA, luciferase reporter assay and CHIP were performed to uncover the underlying mechanism. Furthermore, an in vivo model was carried out to confirm the effect of TAMs on mesenchymal CTC-mediated metastasis. Clinically, CD163+ TAMs infiltrated in invasive front was associated with EMT, mesenchymal CTC ratio, and poor prognosis in patients with CRC. CRC–conditioned macrophages regulated EMT program to enhance CRC cells migration and invasion by secreting IL6. TAMs-derived IL6 activated the JAK2/STAT3 pathway, and activated STAT3 transcriptionally inhibited the tumor suppressor miR-506-3p in CRC cells. miR-506-3p, a key miRNA regulating FoxQ1, was downregulated in CRC cells, resulting in increased FoxQ1 expression, which in turn led to the production of CCL2 that promoted macrophage recruitment. Inhibition of CCL2 or IL6 broke this loop and reduced macrophage migration and mesenchymal CTC-mediated metastasis, respectively. Our data indicates that TAMs induce EMT program to enhance CRC migration, invasion, and CTC-mediated metastasis by regulating the JAK2/STAT3/miR-506-3p/FoxQ1 axis, which in turn leads to the production of CCL2 that promote macrophage recruitment, revealing a new cross-talk between immune cells and tumor cells in CRC microenvironment.
      datePublished:2019-03-30T00:00:00Z
      dateModified:2019-03-30T00:00:00Z
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      pageEnd:23
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      sameAs:https://doi.org/10.1186/s12943-019-0976-4
      keywords:
         Tumor-associated macrophages
         Colorectal cancer
         EMT
         Circulating tumor cell
         Metastasis
         Prognosis
         Cancer Research
         Oncology
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         name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
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         name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
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            address:
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            address:
               name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
               type:PostalAddress
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            address:
               name:Hubei Cancer Clinical Study Center, Wuhan, China
               type:PostalAddress
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            address:
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               type:PostalAddress
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            name:Hubei Key Laboratory of Tumor Biological Behaviors
            address:
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            address:
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            name:Hubei Key Laboratory of Tumor Biological Behaviors
            address:
               name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
               type:PostalAddress
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            address:
               name:Hubei Cancer Clinical Study Center, Wuhan, China
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      affiliation:
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            name:Hubei Key Laboratory of Tumor Biological Behaviors
            address:
               name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
               type:PostalAddress
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            name:Hubei Cancer Clinical Study Center
            address:
               name:Hubei Cancer Clinical Study Center, Wuhan, China
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      name:Xiaobin Lin
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            address:
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               type:PostalAddress
            type:Organization
            name:Hubei Key Laboratory of Tumor Biological Behaviors
            address:
               name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
               type:PostalAddress
            type:Organization
            name:Hubei Cancer Clinical Study Center
            address:
               name:Hubei Cancer Clinical Study Center, Wuhan, China
               type:PostalAddress
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      name:Qing Liu
      affiliation:
            name:Zhongnan Hospital of Wuhan University
            address:
               name:Department of Gastrointestinal Surgery & Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China
               type:PostalAddress
            type:Organization
            name:Hubei Key Laboratory of Tumor Biological Behaviors
            address:
               name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
               type:PostalAddress
            type:Organization
            name:Hubei Cancer Clinical Study Center
            address:
               name:Hubei Cancer Clinical Study Center, Wuhan, China
               type:PostalAddress
            type:Organization
      name:Rongzhang Dou
      affiliation:
            name:Zhongnan Hospital of Wuhan University
            address:
               name:Department of Gastrointestinal Surgery & Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China
               type:PostalAddress
            type:Organization
            name:Hubei Key Laboratory of Tumor Biological Behaviors
            address:
               name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
               type:PostalAddress
            type:Organization
            name:Hubei Cancer Clinical Study Center
            address:
               name:Hubei Cancer Clinical Study Center, Wuhan, China
               type:PostalAddress
            type:Organization
      name:Bin Xiong
      affiliation:
            name:Zhongnan Hospital of Wuhan University
            address:
               name:Department of Gastrointestinal Surgery & Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China
               type:PostalAddress
            type:Organization
            name:Hubei Key Laboratory of Tumor Biological Behaviors
            address:
               name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
               type:PostalAddress
            type:Organization
            name:Hubei Cancer Clinical Study Center
            address:
               name:Hubei Cancer Clinical Study Center, Wuhan, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Gastrointestinal Surgery & Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China
      name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
      name:Hubei Cancer Clinical Study Center, Wuhan, China
      name:Department of Gastrointestinal Surgery & Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China
      name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
      name:Hubei Cancer Clinical Study Center, Wuhan, China
      name:Department of Gastrointestinal Surgery & Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China
      name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
      name:Hubei Cancer Clinical Study Center, Wuhan, China
      name:Department of Gastrointestinal Surgery & Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China
      name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
      name:Hubei Cancer Clinical Study Center, Wuhan, China
      name:Department of Gastrointestinal Surgery & Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China
      name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
      name:Hubei Cancer Clinical Study Center, Wuhan, China
      name:Department of Gastrointestinal Surgery & Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China
      name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
      name:Hubei Cancer Clinical Study Center, Wuhan, China
      name:Department of Gastrointestinal Surgery & Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China
      name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
      name:Hubei Cancer Clinical Study Center, Wuhan, China
      name:Department of Gastrointestinal Surgery & Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China
      name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
      name:Hubei Cancer Clinical Study Center, Wuhan, China
      name:Department of Gastrointestinal Surgery & Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China
      name:Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China
      name:Hubei Cancer Clinical Study Center, Wuhan, China

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