Tumor-promoting macrophages prevail in malignant ascites of advanced gastric cancer
Gastric cancer (GC) patients develop malignant ascites as the disease progresses owing to peritoneal metastasis. GC patients with malignant ascites have a rapidly deteriorating clinical course with short survival following the onset of malignant ascites. Better optimized treatment strategies for thi...
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| Veröffentlicht in: | Experimental & molecular medicine Jg. 52; H. 12; S. 1976 - 1988 |
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| Format: | Journal Article |
| Sprache: | Englisch |
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Nature Publishing Group UK
01.12.2020
Springer Nature B.V 생화학분자생물학회 |
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| ISSN: | 1226-3613, 2092-6413, 2092-6413 |
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| Abstract | Gastric cancer (GC) patients develop malignant ascites as the disease progresses owing to peritoneal metastasis. GC patients with malignant ascites have a rapidly deteriorating clinical course with short survival following the onset of malignant ascites. Better optimized treatment strategies for this subset of patients are needed. To define the cellular characteristics of malignant ascites of GC, we used single-cell RNA sequencing to characterize tumor cells and tumor-associated macrophages (TAMs) from four samples of malignant ascites and one sample of cerebrospinal fluid. Reference transcriptomes for M1 and M2 macrophages were generated by in vitro differentiation of healthy blood-derived monocytes and applied to assess the inflammatory properties of TAMs. We analyzed 180 cells, including tumor cells, macrophages, and mesothelial cells. Dynamic exchange of tumor-promoting signals, including the CCL3–CCR1 or IL1B–IL1R2 interactions, suggests macrophage recruitment and anti-inflammatory tuning by tumor cells. By comparing these data with reference transcriptomes for M1-type and M2-type macrophages, we found noninflammatory characteristics in macrophages recovered from the malignant ascites of GC. Using public datasets, we demonstrated that the single-cell transcriptome-driven M2-specific signature was associated with poor prognosis in GC. Our data indicate that the anti-inflammatory characteristics of TAMs are controlled by tumor cells and present implications for treatment strategies for GC patients in which combination treatment targeting cancer cells and macrophages may have a reciprocal synergistic effect.
Gastric cancer: Understanding cellular interactions suggests potential treatments
New strategies for treating advanced gastric cancer could emerge from insights into the interactions between white blood cells called macrophages and tumor cells in fluid known as malignant ascites that accumulates in the abdomen. Researchers in Seoul, South Korea, led by Hae-Ock Lee at The Catholic University of Korea and Woong-Yang Park at the Samsung Medical Center compared macrophages from healthy subjects with those from gastric cancer ascites. They identified molecular signaling interactions between tumor cells and macrophages that recruited macrophages into the ascites and converted them into more anti-inflammatory forms. The macrophages were then able to promote the activities of the cancer cells. The results suggest that chemicals able to inhibit or deplete proteins now identified as involved in controlling these synergistic interactions could become a new class of therapeutic agents. |
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| AbstractList | Gastric cancer (GC) patients develop malignant ascites as the disease progresses owing to peritoneal metastasis. GC patients with malignant ascites have a rapidly deteriorating clinical course with short survival following the onset of malignant ascites. Better optimized treatment strategies for this subset of patients are needed. To define the cellular characteristics of malignant ascites of GC, we used single-cell RNA sequencing to characterize tumor cells and tumor-associated macrophages (TAMs) from four samples of malignant ascites and one sample of cerebrospinal fluid. Reference transcriptomes for M1 and M2 macrophages were generated by in vitro differentiation of healthy blood-derived monocytes and applied to assess the inflammatory properties of TAMs. We analyzed 180 cells, including tumor cells, macrophages, and mesothelial cells. Dynamic exchange of tumor-promoting signals, including the CCL3–CCR1 or IL1B–IL1R2 interactions, suggests macrophage recruitment and anti-inflammatory tuning by tumor cells. By comparing these data with reference transcriptomes for M1-type and M2-type macrophages, we found noninflammatory characteristics in macrophages recovered from the malignant ascites of GC. Using public datasets, we demonstrated that the single-cell transcriptome-driven M2-specific signature was associated with poor prognosis in GC. Our data indicate that the anti-inflammatory characteristics of TAMs are controlled by tumor cells and present implications for treatment strategies for GC patients in which combination treatment targeting cancer cells and macrophages may have a reciprocal synergistic effect.
Gastric cancer: Understanding cellular interactions suggests potential treatments
New strategies for treating advanced gastric cancer could emerge from insights into the interactions between white blood cells called macrophages and tumor cells in fluid known as malignant ascites that accumulates in the abdomen. Researchers in Seoul, South Korea, led by Hae-Ock Lee at The Catholic University of Korea and Woong-Yang Park at the Samsung Medical Center compared macrophages from healthy subjects with those from gastric cancer ascites. They identified molecular signaling interactions between tumor cells and macrophages that recruited macrophages into the ascites and converted them into more anti-inflammatory forms. The macrophages were then able to promote the activities of the cancer cells. The results suggest that chemicals able to inhibit or deplete proteins now identified as involved in controlling these synergistic interactions could become a new class of therapeutic agents. Gastric cancer (GC) patients develop malignant ascites as the disease progresses owing to peritoneal metastasis. GC patients with malignant ascites have a rapidly deteriorating clinical course with short survival following the onset of malignant ascites. Better optimized treatment strategies for this subset of patients are needed. To define the cellular characteristics of malignant ascites of GC, we used single-cell RNA sequencing to characterize tumor cells and tumor-associated macrophages (TAMs) from four samples of malignant ascites and one sample of cerebrospinal fluid. Reference transcriptomes for M1 and M2 macrophages were generated by in vitro differentiation of healthy blood-derived monocytes and applied to assess the inflammatory properties of TAMs. We analyzed 180 cells, including tumor cells, macrophages, and mesothelial cells. Dynamic exchange of tumor-promoting signals, including the CCL3-CCR1 or IL1B-IL1R2 interactions, suggests macrophage recruitment and anti-inflammatory tuning by tumor cells. By comparing these data with reference transcriptomes for M1-type and M2-type macrophages, we found noninflammatory characteristics in macrophages recovered from the malignant ascites of GC. Using public datasets, we demonstrated that the single-cell transcriptome-driven M2-specific signature was associated with poor prognosis in GC. Our data indicate that the anti-inflammatory characteristics of TAMs are controlled by tumor cells and present implications for treatment strategies for GC patients in which combination treatment targeting cancer cells and macrophages may have a reciprocal synergistic effect. Gastric cancer (GC) patients develop malignant ascites as the disease progresses owing to peritoneal metastasis. GC patients with malignant ascites have a rapidly deteriorating clinical course with short survival following the onset of malignant ascites. Better optimized treatment strategies for this subset of patients are needed. To define the cellular characteristics of malignant ascites of GC, we used single-cell RNA sequencing to characterize tumor cells and tumor-associated macrophages (TAMs) from four samples of malignant ascites and one sample of cerebrospinal fluid. Reference transcriptomes for M1 and M2 macrophages were generated by in vitro differentiation of healthy blood-derived monocytes and applied to assess the inflammatory properties of TAMs. We analyzed 180 cells, including tumor cells, macrophages, and mesothelial cells. Dynamic exchange of tumor-promoting signals, including the CCL3–CCR1 or IL1B–IL1R2 interactions, suggests macrophage recruitment and anti-inflammatory tuning by tumor cells. By comparing these data with reference transcriptomes for M1-type and M2-type macrophages, we found noninflammatory characteristics in macrophages recovered from the malignant ascites of GC. Using public datasets, we demonstrated that the single-cell transcriptome-driven M2-specific signature was associated with poor prognosis in GC. Our data indicate that the anti-inflammatory characteristics of TAMs are controlled by tumor cells and present implications for treatment strategies for GC patients in which combination treatment targeting cancer cells and macrophages may have a reciprocal synergistic effect. KCI Citation Count: 0 Gastric cancer (GC) patients develop malignant ascites as the disease progresses owing to peritoneal metastasis. GC patients with malignant ascites have a rapidly deteriorating clinical course with short survival following the onset of malignant ascites. Better optimized treatment strategies for this subset of patients are needed. To define the cellular characteristics of malignant ascites of GC, we used single-cell RNA sequencing to characterize tumor cells and tumor-associated macrophages (TAMs) from four samples of malignant ascites and one sample of cerebrospinal fluid. Reference transcriptomes for M1 and M2 macrophages were generated by in vitro differentiation of healthy blood-derived monocytes and applied to assess the inflammatory properties of TAMs. We analyzed 180 cells, including tumor cells, macrophages, and mesothelial cells. Dynamic exchange of tumor-promoting signals, including the CCL3–CCR1 or IL1B–IL1R2 interactions, suggests macrophage recruitment and anti-inflammatory tuning by tumor cells. By comparing these data with reference transcriptomes for M1-type and M2-type macrophages, we found noninflammatory characteristics in macrophages recovered from the malignant ascites of GC. Using public datasets, we demonstrated that the single-cell transcriptome-driven M2-specific signature was associated with poor prognosis in GC. Our data indicate that the anti-inflammatory characteristics of TAMs are controlled by tumor cells and present implications for treatment strategies for GC patients in which combination treatment targeting cancer cells and macrophages may have a reciprocal synergistic effect. New strategies for treating advanced gastric cancer could emerge from insights into the interactions between white blood cells called macrophages and tumor cells in fluid known as malignant ascites that accumulates in the abdomen. Researchers in Seoul, South Korea, led by Hae-Ock Lee at The Catholic University of Korea and Woong-Yang Park at the Samsung Medical Center compared macrophages from healthy subjects with those from gastric cancer ascites. They identified molecular signaling interactions between tumor cells and macrophages that recruited macrophages into the ascites and converted them into more anti-inflammatory forms. The macrophages were then able to promote the activities of the cancer cells. The results suggest that chemicals able to inhibit or deplete proteins now identified as involved in controlling these synergistic interactions could become a new class of therapeutic agents. Gastric cancer (GC) patients develop malignant ascites as the disease progresses owing to peritoneal metastasis. GC patients with malignant ascites have a rapidly deteriorating clinical course with short survival following the onset of malignant ascites. Better optimized treatment strategies for this subset of patients are needed. To define the cellular characteristics of malignant ascites of GC, we used single-cell RNA sequencing to characterize tumor cells and tumor-associated macrophages (TAMs) from four samples of malignant ascites and one sample of cerebrospinal fluid. Reference transcriptomes for M1 and M2 macrophages were generated by in vitro differentiation of healthy blood-derived monocytes and applied to assess the inflammatory properties of TAMs. We analyzed 180 cells, including tumor cells, macrophages, and mesothelial cells. Dynamic exchange of tumor-promoting signals, including the CCL3–CCR1 or IL1B–IL1R2 interactions, suggests macrophage recruitment and anti-inflammatory tuning by tumor cells. By comparing these data with reference transcriptomes for M1-type and M2-type macrophages, we found noninflammatory characteristics in macrophages recovered from the malignant ascites of GC. Using public datasets, we demonstrated that the single-cell transcriptome-driven M2-specific signature was associated with poor prognosis in GC. Our data indicate that the anti-inflammatory characteristics of TAMs are controlled by tumor cells and present implications for treatment strategies for GC patients in which combination treatment targeting cancer cells and macrophages may have a reciprocal synergistic effect.Gastric cancer: Understanding cellular interactions suggests potential treatmentsNew strategies for treating advanced gastric cancer could emerge from insights into the interactions between white blood cells called macrophages and tumor cells in fluid known as malignant ascites that accumulates in the abdomen. Researchers in Seoul, South Korea, led by Hae-Ock Lee at The Catholic University of Korea and Woong-Yang Park at the Samsung Medical Center compared macrophages from healthy subjects with those from gastric cancer ascites. They identified molecular signaling interactions between tumor cells and macrophages that recruited macrophages into the ascites and converted them into more anti-inflammatory forms. The macrophages were then able to promote the activities of the cancer cells. The results suggest that chemicals able to inhibit or deplete proteins now identified as involved in controlling these synergistic interactions could become a new class of therapeutic agents. Gastric cancer (GC) patients develop malignant ascites as the disease progresses owing to peritoneal metastasis. GC patients with malignant ascites have a rapidly deteriorating clinical course with short survival following the onset of malignant ascites. Better optimized treatment strategies for this subset of patients are needed. To define the cellular characteristics of malignant ascites of GC, we used single-cell RNA sequencing to characterize tumor cells and tumor-associated macrophages (TAMs) from four samples of malignant ascites and one sample of cerebrospinal fluid. Reference transcriptomes for M1 and M2 macrophages were generated by in vitro differentiation of healthy blood-derived monocytes and applied to assess the inflammatory properties of TAMs. We analyzed 180 cells, including tumor cells, macrophages, and mesothelial cells. Dynamic exchange of tumor-promoting signals, including the CCL3-CCR1 or IL1B-IL1R2 interactions, suggests macrophage recruitment and anti-inflammatory tuning by tumor cells. By comparing these data with reference transcriptomes for M1-type and M2-type macrophages, we found noninflammatory characteristics in macrophages recovered from the malignant ascites of GC. Using public datasets, we demonstrated that the single-cell transcriptome-driven M2-specific signature was associated with poor prognosis in GC. Our data indicate that the anti-inflammatory characteristics of TAMs are controlled by tumor cells and present implications for treatment strategies for GC patients in which combination treatment targeting cancer cells and macrophages may have a reciprocal synergistic effect.Gastric cancer (GC) patients develop malignant ascites as the disease progresses owing to peritoneal metastasis. GC patients with malignant ascites have a rapidly deteriorating clinical course with short survival following the onset of malignant ascites. Better optimized treatment strategies for this subset of patients are needed. To define the cellular characteristics of malignant ascites of GC, we used single-cell RNA sequencing to characterize tumor cells and tumor-associated macrophages (TAMs) from four samples of malignant ascites and one sample of cerebrospinal fluid. Reference transcriptomes for M1 and M2 macrophages were generated by in vitro differentiation of healthy blood-derived monocytes and applied to assess the inflammatory properties of TAMs. We analyzed 180 cells, including tumor cells, macrophages, and mesothelial cells. Dynamic exchange of tumor-promoting signals, including the CCL3-CCR1 or IL1B-IL1R2 interactions, suggests macrophage recruitment and anti-inflammatory tuning by tumor cells. By comparing these data with reference transcriptomes for M1-type and M2-type macrophages, we found noninflammatory characteristics in macrophages recovered from the malignant ascites of GC. Using public datasets, we demonstrated that the single-cell transcriptome-driven M2-specific signature was associated with poor prognosis in GC. Our data indicate that the anti-inflammatory characteristics of TAMs are controlled by tumor cells and present implications for treatment strategies for GC patients in which combination treatment targeting cancer cells and macrophages may have a reciprocal synergistic effect. |
| Author | Eum, Hye Hyeon Jo, Areum Kim, Nayoung Kwon, Minsuk Lee, Hae-Ock Lee, Jeeyun Kim, Seung Tae Park, Woong-Yang Son, Dae-Soon Ryu, Daeun Chung, Woosung Hong, Yourae |
| Author_xml | – sequence: 1 givenname: Hye Hyeon orcidid: 0000-0002-8081-4121 surname: Eum fullname: Eum, Hye Hyeon organization: Samsung Genome Institute, Samsung Medical Center – sequence: 2 givenname: Minsuk orcidid: 0000-0003-1833-6576 surname: Kwon fullname: Kwon, Minsuk organization: Division of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine – sequence: 3 givenname: Daeun surname: Ryu fullname: Ryu, Daeun organization: Samsung Genome Institute, Samsung Medical Center – sequence: 4 givenname: Areum orcidid: 0000-0001-7815-8439 surname: Jo fullname: Jo, Areum organization: Samsung Genome Institute, Samsung Medical Center – sequence: 5 givenname: Woosung surname: Chung fullname: Chung, Woosung organization: Samsung Genome Institute, Samsung Medical Center – sequence: 6 givenname: Nayoung orcidid: 0000-0003-3202-750X surname: Kim fullname: Kim, Nayoung organization: Samsung Genome Institute, Samsung Medical Center – sequence: 7 givenname: Yourae surname: Hong fullname: Hong, Yourae organization: Samsung Genome Institute, Samsung Medical Center, Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences & Technology, Sungkyunkwan University – sequence: 8 givenname: Dae-Soon surname: Son fullname: Son, Dae-Soon organization: School of Big Data Science, Data Science Convergence Research Center, Hallym University – sequence: 9 givenname: Seung Tae surname: Kim fullname: Kim, Seung Tae organization: Division of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine – sequence: 10 givenname: Jeeyun surname: Lee fullname: Lee, Jeeyun organization: Division of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine – sequence: 11 givenname: Hae-Ock orcidid: 0000-0001-5123-0322 surname: Lee fullname: Lee, Hae-Ock email: haeocklee@catholic.ac.kr organization: Department of Biomedicine and Health Sciences, Graduate School of The Catholic University of Korea – sequence: 12 givenname: Woong-Yang orcidid: 0000-0003-4234-0380 surname: Park fullname: Park, Woong-Yang email: woongyang.park@samsung.com organization: Samsung Genome Institute, Samsung Medical Center, School of Big Data Science, Data Science Convergence Research Center, Hallym University, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33277616$$D View this record in MEDLINE/PubMed https://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART002654532$$DAccess content in National Research Foundation of Korea (NRF) |
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| SubjectTerms | 38/39 45/91 631/208/514/1949 631/208/69 631/67/1504/1829 Ascites Ascites - pathology Biomedical and Life Sciences Biomedicine Case-Control Studies CCL3 protein CCR1 protein Cell Communication Cell Plasticity - immunology Cerebrospinal fluid Gastric cancer Gene expression Gene Expression Profiling Gene Expression Regulation, Neoplastic High-Throughput Nucleotide Sequencing Humans Inflammation Interleukin 1 Leukocytes Macrophages Macrophages - immunology Macrophages - metabolism Medical Biochemistry Medical prognosis Metastases Molecular Medicine Monocytes Patients Peritoneal Neoplasms - mortality Peritoneal Neoplasms - pathology Peritoneal Neoplasms - secondary Peritoneum Prognosis Ribonucleic acid RNA Signal Transduction Single-Cell Analysis Stem Cells Stomach Neoplasms - mortality Stomach Neoplasms - pathology Transcriptome Transcriptomes Tumor cells Tumor Microenvironment - immunology 생화학 |
| Title | Tumor-promoting macrophages prevail in malignant ascites of advanced gastric cancer |
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