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We are analyzing https://link.springer.com/article/10.1186/s13045-020-00887-1.

Title:
Oct4 promotes M2 macrophage polarization through upregulation of macrophage colony-stimulating factor in lung cancer | Journal of Hematology & Oncology
Description:
Background Expression of Oct4 maintains cancer stem cell (CSC)-like properties in lung cancer cells and is correlated with poor prognosis of lung adenocarcinoma. M2-type tumor-associated macrophages (TAMs) promote cancer cell migration and metastasis. Tumor microenvironments promote monocyte differentiation into M2 TAMs via a complex cytokine-based connection. We explored the role of Oct4 in cytokine secretion in lung cancer and its impact on M2 TAM polarization. Methods Monocytes co-cultured with the conditioned medium from Oct4-overexpressing lung cancer cells were used to investigate M2 TAM differentiation. The inflammatory factors in the conditioned medium of Oct4-overexpressing A549 cells were examined using human inflammation antibody arrays. The correlations of Oct4, macrophage colony-stimulating factor (M-CSF), and M2 TAMs were validated in lung cancer cells, syngeneic mouse lung tumor models, and clinical samples of non-small cell lung cancer (NSCLC). Results Oct4-overexpressing A549 cells expressed elevated levels of M-CSF, which contributed to increased M2 macrophages and enhanced tumor migration. Overexpression of Oct4 enhanced tumor growth and reduced the survival of lung tumor-bearing mice, which was correlated with increased number of M2 macrophages in lung cancer. Notably, NSCLC patients with high expression levels of Oct4, M-CSF, and M2 TAMs had the poorest recurrence-free survival. A positive correlation between Oct4, M-CSF, and M2 TAMs was observed in the tumor tissue of NSCLC patient. Treatment with all-trans retinoic acid exerted anti-tumor effects and reduced M2 TAMs in tumor-bearing mice. Conclusions Our results indicate that Oct4 expressed by lung cancer cells promotes M2 macrophage polarization through upregulation of M-CSF secretion, leading to cancer growth and metastasis. Our findings also implicate that the Oct4/M-CSF axis in M2 macrophage polarization may be potential therapeutic targets for lung cancer.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

cells, cancer, oct, lung, tumor, mcsf, pubmed, macrophages, article, expression, google, scholar, cell, cas, fig, macrophage, mice, control, patients, human, levels, tumors, atra, promoter, central, results, vector, analysis, metastasis, tams, conditioned, medium, survival, luciferase, ore, growth, study, taiwan, stem, additional, aoct, data, polarization, factor, adenocarcinoma, treatment, progression, shown, tnfα, obtained,

Topics {✒️}

tumor-derived chemokine mcp-1/ccl2 pfrl2-m-csf-ore1mut-ore2mut macrophage colony-stimulating factor cancer-related mortality worldwide retinoid acid-responsive elements generate pfrl2-m-csf-ore1mut nf-κb inhibitor jsh-23 mouse anti-oct4 antibody enzyme-linked immunosorbent assay stable oct4-overexpressing a549 article download pdf tlr4/il-10 signaling pathway human glyceraldehyde-3-phosphate dehydrogenase gia-shing shieh anti-igg antibody combined tumor necrosis factor-alpha targeting tumor-infiltrating macrophages anti-m-csf antibody chi-mei medical center 1-puro-based lentiviral vectors tumor necrosis factor-α trans retinoic acid psin-ef-oct4-pur complex cytokine-based connection oct4-expressing cancer cells full size image psin-ef2-oct4-pur ethidium bromide-stained gels lung tumor-bearing mice cl1-5-f4 cell lines colony-stimulating factor-1 macrophage-cancer cell interaction oct4-overexpressing a549 cells kaplan-meier analysis shows ll2 tumor-bearing mice oct4-overexpressing a549-oct4 m-csf promoter carrying generate m1-polarized cells oncolytic adenovirus carrying pfrl2-m-csf-ore2mut yi-ting yen control vector psin-null m1/m2 gene signatures kaplan-meier survival method pfrl2-m-csf construct m-csf promoter required oct4-knockdown a549 cells macrophage-mediated promotion retinoic acid syndrome promoted tumor metastasis

Schema {🗺️}

WebPage:
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         headline:Oct4 promotes M2 macrophage polarization through upregulation of macrophage colony-stimulating factor in lung cancer
         description:Expression of Oct4 maintains cancer stem cell (CSC)-like properties in lung cancer cells and is correlated with poor prognosis of lung adenocarcinoma. M2-type tumor-associated macrophages (TAMs) promote cancer cell migration and metastasis. Tumor microenvironments promote monocyte differentiation into M2 TAMs via a complex cytokine-based connection. We explored the role of Oct4 in cytokine secretion in lung cancer and its impact on M2 TAM polarization. Monocytes co-cultured with the conditioned medium from Oct4-overexpressing lung cancer cells were used to investigate M2 TAM differentiation. The inflammatory factors in the conditioned medium of Oct4-overexpressing A549 cells were examined using human inflammation antibody arrays. The correlations of Oct4, macrophage colony-stimulating factor (M-CSF), and M2 TAMs were validated in lung cancer cells, syngeneic mouse lung tumor models, and clinical samples of non-small cell lung cancer (NSCLC). Oct4-overexpressing A549 cells expressed elevated levels of M-CSF, which contributed to increased M2 macrophages and enhanced tumor migration. Overexpression of Oct4 enhanced tumor growth and reduced the survival of lung tumor-bearing mice, which was correlated with increased number of M2 macrophages in lung cancer. Notably, NSCLC patients with high expression levels of Oct4, M-CSF, and M2 TAMs had the poorest recurrence-free survival. A positive correlation between Oct4, M-CSF, and M2 TAMs was observed in the tumor tissue of NSCLC patient. Treatment with all-trans retinoic acid exerted anti-tumor effects and reduced M2 TAMs in tumor-bearing mice. Our results indicate that Oct4 expressed by lung cancer cells promotes M2 macrophage polarization through upregulation of M-CSF secretion, leading to cancer growth and metastasis. Our findings also implicate that the Oct4/M-CSF axis in M2 macrophage polarization may be potential therapeutic targets for lung cancer.
         datePublished:2020-06-01T00:00:00Z
         dateModified:2020-06-01T00:00:00Z
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            Lung cancer
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      headline:Oct4 promotes M2 macrophage polarization through upregulation of macrophage colony-stimulating factor in lung cancer
      description:Expression of Oct4 maintains cancer stem cell (CSC)-like properties in lung cancer cells and is correlated with poor prognosis of lung adenocarcinoma. M2-type tumor-associated macrophages (TAMs) promote cancer cell migration and metastasis. Tumor microenvironments promote monocyte differentiation into M2 TAMs via a complex cytokine-based connection. We explored the role of Oct4 in cytokine secretion in lung cancer and its impact on M2 TAM polarization. Monocytes co-cultured with the conditioned medium from Oct4-overexpressing lung cancer cells were used to investigate M2 TAM differentiation. The inflammatory factors in the conditioned medium of Oct4-overexpressing A549 cells were examined using human inflammation antibody arrays. The correlations of Oct4, macrophage colony-stimulating factor (M-CSF), and M2 TAMs were validated in lung cancer cells, syngeneic mouse lung tumor models, and clinical samples of non-small cell lung cancer (NSCLC). Oct4-overexpressing A549 cells expressed elevated levels of M-CSF, which contributed to increased M2 macrophages and enhanced tumor migration. Overexpression of Oct4 enhanced tumor growth and reduced the survival of lung tumor-bearing mice, which was correlated with increased number of M2 macrophages in lung cancer. Notably, NSCLC patients with high expression levels of Oct4, M-CSF, and M2 TAMs had the poorest recurrence-free survival. A positive correlation between Oct4, M-CSF, and M2 TAMs was observed in the tumor tissue of NSCLC patient. Treatment with all-trans retinoic acid exerted anti-tumor effects and reduced M2 TAMs in tumor-bearing mice. Our results indicate that Oct4 expressed by lung cancer cells promotes M2 macrophage polarization through upregulation of M-CSF secretion, leading to cancer growth and metastasis. Our findings also implicate that the Oct4/M-CSF axis in M2 macrophage polarization may be potential therapeutic targets for lung cancer.
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      dateModified:2020-06-01T00:00:00Z
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         Lung cancer
         Oct4
         M2 macrophage
         Tumor-associated macrophage
         M-CSF
         Oncology
         Hematology
         Cancer Research
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      author:
            name:Chia-Sing Lu
            affiliation:
                  name:College of Medicine, National Cheng Kung University
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                     type:PostalAddress
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            name:Ai-Li Shiau
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                     type:PostalAddress
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                  name:College of Medicine, National Cheng Kung University
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            name:Yin-Hsun Feng
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                     name:Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
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            type:Organization
      name:Tsui-Shan Hsu
      affiliation:
            name:College of Medicine, National Cheng Kung University
            address:
               name:Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      name:Chung-Teng Wang
      affiliation:
            name:College of Medicine, National Cheng Kung University
            address:
               name:Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      name:Yu-Chu Su
      affiliation:
            name:College of Medicine, National Cheng Kung University
            address:
               name:Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      name:Ming-Shian Tsai
      affiliation:
            name:College of Medicine, National Cheng Kung University
            address:
               name:Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      name:Yin-Hsun Feng
      affiliation:
            name:Chi-Mei Medical Center
            address:
               name:Division of Hematology and Oncology, Department of Internal Medicine, Chi-Mei Medical Center, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      name:Yau-Lin Tseng
      affiliation:
            name:College of Medicine, National Cheng Kung University
            address:
               name:Division of Thoracic Surgery, Department of Surgery, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      name:Yi-Ting Yen
      affiliation:
            name:College of Medicine, National Cheng Kung University
            address:
               name:Division of Thoracic Surgery, Department of Surgery, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      name:Chao-Liang Wu
      affiliation:
            name:College of Medicine, National Cheng Kung University
            address:
               name:Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      name:Gia-Shing Shieh
      url:http://orcid.org/0000-0003-2480-4313
      affiliation:
            name:College of Medicine, National Cheng Kung University
            address:
               name:Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
            name:Tainan Hospital, Ministry of Health and Welfare, Executive Yuan
            address:
               name:Department of Urology, Tainan Hospital, Ministry of Health and Welfare, Executive Yuan, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan
      name:Division of Thoracic Surgery, Department of Surgery, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Division of Hematology and Oncology, Department of Internal Medicine, Chi-Mei Medical Center, Tainan, Taiwan
      name:Division of Thoracic Surgery, Department of Surgery, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Division of Thoracic Surgery, Department of Surgery, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Department of Urology, Tainan Hospital, Ministry of Health and Welfare, Executive Yuan, Tainan, Taiwan

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