Expression profiles and function of IL6 in polymorphonuclear myeloid-derived suppressor cells
IL6 is an inflammatory cytokine with pleiotropic functions in both immune and nonimmune cells, and its expression level is inversely correlated with disease prognosis in patients with cancer. However, blocking IL6 alone has only yielded minimal efficacy in human cancer patients. We aimed at defining...
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Published in | Cancer Immunology, Immunotherapy Vol. 69; no. 11; pp. 2233 - 2245 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.11.2020
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Abstract | IL6 is an inflammatory cytokine with pleiotropic functions in both immune and nonimmune cells, and its expression level is inversely correlated with disease prognosis in patients with cancer. However, blocking IL6 alone has only yielded minimal efficacy in human cancer patients. We aimed at defining IL6 expression profiles under inflammatory conditions and cancer, and elucidating the mechanism underlying IL6 intrinsic signaling in colon carcinoma. We report here that colonic inflammation induces IL6 expression primarily in the CD11b
+
Ly6G
+
Ly6C
lo
polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) in colon. Although both tumor cells, T cells and myeloid cells all express IL6, PMN-MDSCs are the primary cell type that express IL6 in colon carcinoma, suggesting that IL6 up-regulation is a response to inflammation in colon epithelium and tumor microenvironment. Furthermore, we determined that IL6 activates STAT3 to up-regulate DNMT1 and DNMT3b expression in colon tumor cells, thereby revealing an epigenetic mechanism that mediates the IL6-STAT3 signaling pathway in colon carcinoma. Surprisingly, knocking out IL6 in colon tumor cells did not significantly alter tumor growth in WT mice. Conversely, IL6-sufficient colon and pancreatic tumor grow at similar rate in WT and IL6-deficient mice. However, overexpression of IL6 in colon tumor cells significantly increases tumor growth in vivo. Our findings determine that a high tumor local IL6 threshold is essential for IL6 function in colon tumor promotion and targeting the IL6-expressing PMN-MDSCs is potentially an effective approach to suppress colon tumor growth in vivo. |
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AbstractList | IL6 is an inflammatory cytokine with pleiotropic functions in both immune and nonimmune cells, and its expression level is inversely correlated with disease prognosis in patients with cancer. However, blocking IL6 alone has only yielded minimal efficacy in human cancer patients. We aimed at defining IL6 expression profiles under inflammatory conditions and cancer, and elucidating the mechanism underlying IL6 intrinsic signaling in colon carcinoma. We report here that colonic inflammation induces IL6 expression primarily in the CD11b
Ly6G
Ly6C
polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) in colon. Although both tumor cells, T cells and myeloid cells all express IL6, PMN-MDSCs are the primary cell type that express IL6 in colon carcinoma, suggesting that IL6 up-regulation is a response to inflammation in colon epithelium and tumor microenvironment. Furthermore, we determined that IL6 activates STAT3 to up-regulate DNMT1 and DNMT3b expression in colon tumor cells, thereby revealing an epigenetic mechanism that mediates the IL6-STAT3 signaling pathway in colon carcinoma. Surprisingly, knocking out IL6 in colon tumor cells did not significantly alter tumor growth in WT mice. Conversely, IL6-sufficient colon and pancreatic tumor grow at similar rate in WT and IL6-deficient mice. However, overexpression of IL6 in colon tumor cells significantly increases tumor growth in vivo. Our findings determine that a high tumor local IL6 threshold is essential for IL6 function in colon tumor promotion and targeting the IL6-expressing PMN-MDSCs is potentially an effective approach to suppress colon tumor growth in vivo. IL6 is an inflammatory cytokine with pleiotropic functions in both immune and nonimmune cells, and its expression level is inversely correlated with disease prognosis in patients with cancer. However, blocking IL6 alone has only yielded minimal efficacy in human cancer patients. We aimed at defining IL6 expression profiles under inflammatory conditions and cancer, and elucidating the mechanism underlying IL6 intrinsic signaling in colon carcinoma. We report here that colonic inflammation induces IL6 expression primarily in the CD11b + Ly6G + Ly6C lo polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) in colon. Although both tumor cells, T cells and myeloid cells all express IL6, PMN-MDSCs are the primary cell type that express IL6 in colon carcinoma, suggesting that IL6 up-regulation is a response to inflammation in colon epithelium and tumor microenvironment. Furthermore, we determined that IL6 activates STAT3 to up-regulate DNMT1 and DNMT3b expression in colon tumor cells, thereby revealing an epigenetic mechanism that mediates the IL6-STAT3 signaling pathway in colon carcinoma. Surprisingly, knocking out IL6 in colon tumor cells did not significantly alter tumor growth in WT mice. Conversely, IL6-sufficient colon and pancreatic tumor grow at similar rate in WT and IL6-deficient mice. However, overexpression of IL6 in colon tumor cells significantly increases tumor growth in vivo. Our findings determine that a high tumor local IL6 threshold is essential for IL6 function in colon tumor promotion and targeting the IL6-expressing PMN-MDSCs is potentially an effective approach to suppress colon tumor growth in vivo. IL6 is an inflammatory cytokine with pleiotropic functions in both immune and nonimmune cells, and its expression level is inversely correlated with disease prognosis in patients with cancer. However, blocking IL6 alone has only yielded minimal efficacy in human cancer patients. We aimed at defining IL6 expression profiles under inflammatory conditions and cancer, and elucidating the mechanism underlying IL6 intrinsic signaling in colon carcinoma. We report here that colonic inflammation induces IL6 expression primarily in the CD11b+Ly6G+Ly6Clo polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) in colon. Although both tumor cells, T cells and myeloid cells all express IL6, PMN-MDSCs are the primary cell type that express IL6 in colon carcinoma, suggesting that IL6 up-regulation is a response to inflammation in colon epithelium and tumor microenvironment. Furthermore, we determined that IL6 activates STAT3 to up-regulate DNMT1 and DNMT3b expression in colon tumor cells, thereby revealing an epigenetic mechanism that mediates the IL6-STAT3 signaling pathway in colon carcinoma. Surprisingly, knocking out IL6 in colon tumor cells did not significantly alter tumor growth in WT mice. Conversely, IL6-sufficient colon and pancreatic tumor grow at similar rate in WT and IL6-deficient mice. However, overexpression of IL6 in colon tumor cells significantly increases tumor growth in vivo. Our findings determine that a high tumor local IL6 threshold is essential for IL6 function in colon tumor promotion and targeting the IL6-expressing PMN-MDSCs is potentially an effective approach to suppress colon tumor growth in vivo. |
Author | Redd, Priscilla S. Ibrahim, Mohammed L. Lu, Chunwan Smith, Alyssa D. Yang, Dafeng Liu, Kebin Klement, John D. |
Author_xml | – sequence: 1 givenname: Mohammed L. surname: Ibrahim fullname: Ibrahim, Mohammed L. organization: Department of Biochemistry and Molecular Biology, Medical College of Georgia, Georgia Cancer Center, Medical College of Georgia, Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, Cairo University – sequence: 2 givenname: Chunwan surname: Lu fullname: Lu, Chunwan organization: Department of Biochemistry and Molecular Biology, Medical College of Georgia, Georgia Cancer Center, Medical College of Georgia, Charlie Norwood VA Medical Center – sequence: 3 givenname: John D. surname: Klement fullname: Klement, John D. organization: Department of Biochemistry and Molecular Biology, Medical College of Georgia, Georgia Cancer Center, Medical College of Georgia, Charlie Norwood VA Medical Center – sequence: 4 givenname: Priscilla S. surname: Redd fullname: Redd, Priscilla S. organization: Department of Biochemistry and Molecular Biology, Medical College of Georgia, Georgia Cancer Center, Medical College of Georgia, Charlie Norwood VA Medical Center – sequence: 5 givenname: Dafeng surname: Yang fullname: Yang, Dafeng organization: Department of Biochemistry and Molecular Biology, Medical College of Georgia, Georgia Cancer Center, Medical College of Georgia, Charlie Norwood VA Medical Center – sequence: 6 givenname: Alyssa D. surname: Smith fullname: Smith, Alyssa D. organization: Department of Biochemistry and Molecular Biology, Medical College of Georgia, Georgia Cancer Center, Medical College of Georgia, Charlie Norwood VA Medical Center – sequence: 7 givenname: Kebin orcidid: 0000-0003-1965-7240 surname: Liu fullname: Liu, Kebin email: Kliu@augusta.edu organization: Department of Biochemistry and Molecular Biology, Medical College of Georgia, Georgia Cancer Center, Medical College of Georgia, Charlie Norwood VA Medical Center |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32488308$$D View this record in MEDLINE/PubMed |
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Keywords | Colon tumor DNMT MDSCs IL6 Colonic inflammation STAT3 |
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SubjectTerms | Adenocarcinoma - immunology Adenocarcinoma - pathology Animals Cancer Research Colorectal Neoplasms - immunology Colorectal Neoplasms - pathology Gene Expression Regulation, Neoplastic - physiology Humans Immunology Interleukin-6 - immunology Interleukin-6 - metabolism Medicine Medicine & Public Health Mice Mice, Inbred BALB C Myeloid-Derived Suppressor Cells - immunology Myeloid-Derived Suppressor Cells - metabolism Oncology Original Original Article Signal Transduction - immunology Transcriptome Tumor Microenvironment - immunology |
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Title | Expression profiles and function of IL6 in polymorphonuclear myeloid-derived suppressor cells |
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