Construction of TME and Identification of crosstalk between malignant cells and macrophages by SPP1 in hepatocellular carcinoma
Liver cancer accounts for 6% of all malignancies causing death worldwide, and hepatocellular carcinoma (HCC) is the most common histological type. HCC is a heterogeneous cancer, but how the tumour microenvironment (TME) of HCC contributes to the progression of HCC remains unclear. In this study, we...
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| Veröffentlicht in: | Cancer Immunology, Immunotherapy Immunotherapy, 2022-01, Vol.71 (1), p.121-136 |
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| container_title | Cancer Immunology, Immunotherapy |
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| creator | Liu, Lulu Zhang, Ruyi Deng, Jingwen Dai, Xiaomeng Zhu, Xudong Fu, Qihan Zhang, Hangyu Tong, Zhou Zhao, Peng Fang, Weijia Zheng, Yi Bao, Xuanwen |
| description | Liver cancer accounts for 6% of all malignancies causing death worldwide, and hepatocellular carcinoma (HCC) is the most common histological type. HCC is a heterogeneous cancer, but how the tumour microenvironment (TME) of HCC contributes to the progression of HCC remains unclear. In this study, we investigated the immune microenvironment by multiomics analysis. The tumour immune infiltration characteristics of HCC were determined at the genomic, epigenetic, bulk transcriptome and single-cell levels by data from The Cancer Genome Atlas portal and the Gene Expression Omnibus (GEO). An epigenetic immune-related scoring system (EIRS) was developed to stratify patients with poor prognosis. SPP1, one gene in the EIRS system, was identified as an immune-related predictor of poor survival in HCC patients. Through receptor-ligand pair analysis in single-cell RNA-seq, SPP1 was indicated to mediate the crosstalk between HCC cells and macrophages via SPP1-CD44 and SPP1-PTGER4 association. In vitro experiments further validate SPP1 can trigger the polarization of macrophages to M2-phenotype tumour-associated macrophages (TAMs). |
| doi_str_mv | 10.1007/s00262-021-02967-8 |
| format | Article |
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HCC is a heterogeneous cancer, but how the tumour microenvironment (TME) of HCC contributes to the progression of HCC remains unclear. In this study, we investigated the immune microenvironment by multiomics analysis. The tumour immune infiltration characteristics of HCC were determined at the genomic, epigenetic, bulk transcriptome and single-cell levels by data from The Cancer Genome Atlas portal and the Gene Expression Omnibus (GEO). An epigenetic immune-related scoring system (EIRS) was developed to stratify patients with poor prognosis. SPP1, one gene in the EIRS system, was identified as an immune-related predictor of poor survival in HCC patients. Through receptor-ligand pair analysis in single-cell RNA-seq, SPP1 was indicated to mediate the crosstalk between HCC cells and macrophages via SPP1-CD44 and SPP1-PTGER4 association. In vitro experiments further validate SPP1 can trigger the polarization of macrophages to M2-phenotype tumour-associated macrophages (TAMs).</description><identifier>ISSN: 0340-7004</identifier><identifier>EISSN: 1432-0851</identifier><identifier>DOI: 10.1007/s00262-021-02967-8</identifier><identifier>PMID: 34028567</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adult ; Aged ; Algorithms ; Cancer Research ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; CD44 antigen ; Cell Line, Tumor ; Cell Movement ; Coculture Techniques ; Disease-Free Survival ; DNA Methylation ; Epigenetics ; Female ; Gene expression ; Genome, Human ; Hep G2 Cells ; Hepatocellular carcinoma ; Humans ; Immune System ; Immunology ; Immunotherapy ; Ligands ; Liver cancer ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Macrophages ; Macrophages - metabolism ; Male ; Medical prognosis ; Medicine ; Medicine & Public Health ; Metastases ; Microenvironments ; Middle Aged ; Monocytes - metabolism ; Oncology ; Original ; Original Article ; Osteopontin - metabolism ; Phenotype ; Phenotypes ; Prognosis ; RNA, Small Interfering - metabolism ; Transcriptomes ; Treatment Outcome ; Tumor Microenvironment ; Tumors</subject><ispartof>Cancer Immunology, Immunotherapy, 2022-01, Vol.71 (1), p.121-136</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c431t-13ab6de3b06eed798f013df748a355d7efd62d9a156a27dfa729410e8832951b3</citedby><cites>FETCH-LOGICAL-c431t-13ab6de3b06eed798f013df748a355d7efd62d9a156a27dfa729410e8832951b3</cites><orcidid>0000-0002-7066-2937 ; 0000-0002-6232-3783</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10992184/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10992184/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,41493,42562,51324,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34028567$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Lulu</creatorcontrib><creatorcontrib>Zhang, Ruyi</creatorcontrib><creatorcontrib>Deng, Jingwen</creatorcontrib><creatorcontrib>Dai, Xiaomeng</creatorcontrib><creatorcontrib>Zhu, Xudong</creatorcontrib><creatorcontrib>Fu, Qihan</creatorcontrib><creatorcontrib>Zhang, Hangyu</creatorcontrib><creatorcontrib>Tong, Zhou</creatorcontrib><creatorcontrib>Zhao, Peng</creatorcontrib><creatorcontrib>Fang, Weijia</creatorcontrib><creatorcontrib>Zheng, Yi</creatorcontrib><creatorcontrib>Bao, Xuanwen</creatorcontrib><title>Construction of TME and Identification of crosstalk between malignant cells and macrophages by SPP1 in hepatocellular carcinoma</title><title>Cancer Immunology, Immunotherapy</title><addtitle>Cancer Immunol Immunother</addtitle><addtitle>Cancer Immunol Immunother</addtitle><description>Liver cancer accounts for 6% of all malignancies causing death worldwide, and hepatocellular carcinoma (HCC) is the most common histological type. HCC is a heterogeneous cancer, but how the tumour microenvironment (TME) of HCC contributes to the progression of HCC remains unclear. In this study, we investigated the immune microenvironment by multiomics analysis. The tumour immune infiltration characteristics of HCC were determined at the genomic, epigenetic, bulk transcriptome and single-cell levels by data from The Cancer Genome Atlas portal and the Gene Expression Omnibus (GEO). An epigenetic immune-related scoring system (EIRS) was developed to stratify patients with poor prognosis. SPP1, one gene in the EIRS system, was identified as an immune-related predictor of poor survival in HCC patients. Through receptor-ligand pair analysis in single-cell RNA-seq, SPP1 was indicated to mediate the crosstalk between HCC cells and macrophages via SPP1-CD44 and SPP1-PTGER4 association. In vitro experiments further validate SPP1 can trigger the polarization of macrophages to M2-phenotype tumour-associated macrophages (TAMs).</description><subject>Adult</subject><subject>Aged</subject><subject>Algorithms</subject><subject>Cancer Research</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>CD44 antigen</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Coculture Techniques</subject><subject>Disease-Free Survival</subject><subject>DNA Methylation</subject><subject>Epigenetics</subject><subject>Female</subject><subject>Gene expression</subject><subject>Genome, Human</subject><subject>Hep G2 Cells</subject><subject>Hepatocellular carcinoma</subject><subject>Humans</subject><subject>Immune System</subject><subject>Immunology</subject><subject>Immunotherapy</subject><subject>Ligands</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - pathology</subject><subject>Macrophages</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastases</subject><subject>Microenvironments</subject><subject>Middle Aged</subject><subject>Monocytes - metabolism</subject><subject>Oncology</subject><subject>Original</subject><subject>Original Article</subject><subject>Osteopontin - metabolism</subject><subject>Phenotype</subject><subject>Phenotypes</subject><subject>Prognosis</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Transcriptomes</subject><subject>Treatment Outcome</subject><subject>Tumor Microenvironment</subject><subject>Tumors</subject><issn>0340-7004</issn><issn>1432-0851</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kU9v1DAQxS0EoqXwBTggS1y4BDy2EzsnhFYFKhVRiXK2JrGz65LYi50U9cRXx7vblj8HDpatmd88-_kR8hzYa2BMvcmM8YZXjENZbaMq_YAcgxSlpGt4SI6ZkKxSjMkj8iTnq3LgrG0fk6NS57pu1DH5uYohz2npZx8DjQO9_HRKMVh6Zl2Y_eB7vOv0KeY84_iNdm7-4VygE45-HTDMtHfjmPdzExZuu8G1y7S7oV8uLoD6QDdui3PcYcuIifaYeh_ihE_JowHH7J7d7ifk6_vTy9XH6vzzh7PVu_OqlwLmCgR2jXWiY41zVrV6YCDsoKRGUddWucE23LYIdYNc2QEVbyUwp7XgbQ2dOCFvD7rbpZuc7Yu5hKPZJj9hujERvfm7E_zGrOO1gfJjHLQsCq9uFVL8vrg8m8nnnSEMLi7Z8FpALWStWUFf_oNexSWF4s_wBhSAlC0Uih-o_ccmN9y_BpjZBWwOAZsSsNkHbHQZevGnj_uRu0QLIA5ALq2wdun33f-R_QXjj7Lp</recordid><startdate>20220101</startdate><enddate>20220101</enddate><creator>Liu, Lulu</creator><creator>Zhang, Ruyi</creator><creator>Deng, Jingwen</creator><creator>Dai, Xiaomeng</creator><creator>Zhu, Xudong</creator><creator>Fu, Qihan</creator><creator>Zhang, Hangyu</creator><creator>Tong, Zhou</creator><creator>Zhao, Peng</creator><creator>Fang, Weijia</creator><creator>Zheng, Yi</creator><creator>Bao, Xuanwen</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7066-2937</orcidid><orcidid>https://orcid.org/0000-0002-6232-3783</orcidid></search><sort><creationdate>20220101</creationdate><title>Construction of TME and Identification of crosstalk between malignant cells and macrophages by SPP1 in hepatocellular carcinoma</title><author>Liu, Lulu ; Zhang, Ruyi ; Deng, Jingwen ; Dai, Xiaomeng ; Zhu, Xudong ; Fu, Qihan ; Zhang, Hangyu ; Tong, Zhou ; Zhao, Peng ; Fang, Weijia ; Zheng, Yi ; Bao, Xuanwen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c431t-13ab6de3b06eed798f013df748a355d7efd62d9a156a27dfa729410e8832951b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Algorithms</topic><topic>Cancer Research</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>CD44 antigen</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Coculture Techniques</topic><topic>Disease-Free Survival</topic><topic>DNA Methylation</topic><topic>Epigenetics</topic><topic>Female</topic><topic>Gene expression</topic><topic>Genome, Human</topic><topic>Hep G2 Cells</topic><topic>Hepatocellular carcinoma</topic><topic>Humans</topic><topic>Immune System</topic><topic>Immunology</topic><topic>Immunotherapy</topic><topic>Ligands</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - pathology</topic><topic>Macrophages</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metastases</topic><topic>Microenvironments</topic><topic>Middle Aged</topic><topic>Monocytes - metabolism</topic><topic>Oncology</topic><topic>Original</topic><topic>Original Article</topic><topic>Osteopontin - metabolism</topic><topic>Phenotype</topic><topic>Phenotypes</topic><topic>Prognosis</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Transcriptomes</topic><topic>Treatment Outcome</topic><topic>Tumor Microenvironment</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Lulu</creatorcontrib><creatorcontrib>Zhang, Ruyi</creatorcontrib><creatorcontrib>Deng, Jingwen</creatorcontrib><creatorcontrib>Dai, Xiaomeng</creatorcontrib><creatorcontrib>Zhu, Xudong</creatorcontrib><creatorcontrib>Fu, Qihan</creatorcontrib><creatorcontrib>Zhang, Hangyu</creatorcontrib><creatorcontrib>Tong, Zhou</creatorcontrib><creatorcontrib>Zhao, Peng</creatorcontrib><creatorcontrib>Fang, Weijia</creatorcontrib><creatorcontrib>Zheng, Yi</creatorcontrib><creatorcontrib>Bao, Xuanwen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer Immunology, Immunotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Lulu</au><au>Zhang, Ruyi</au><au>Deng, Jingwen</au><au>Dai, Xiaomeng</au><au>Zhu, Xudong</au><au>Fu, Qihan</au><au>Zhang, Hangyu</au><au>Tong, Zhou</au><au>Zhao, Peng</au><au>Fang, Weijia</au><au>Zheng, Yi</au><au>Bao, Xuanwen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Construction of TME and Identification of crosstalk between malignant cells and macrophages by SPP1 in hepatocellular carcinoma</atitle><jtitle>Cancer Immunology, Immunotherapy</jtitle><stitle>Cancer Immunol Immunother</stitle><addtitle>Cancer Immunol Immunother</addtitle><date>2022-01-01</date><risdate>2022</risdate><volume>71</volume><issue>1</issue><spage>121</spage><epage>136</epage><pages>121-136</pages><issn>0340-7004</issn><eissn>1432-0851</eissn><abstract>Liver cancer accounts for 6% of all malignancies causing death worldwide, and hepatocellular carcinoma (HCC) is the most common histological type. HCC is a heterogeneous cancer, but how the tumour microenvironment (TME) of HCC contributes to the progression of HCC remains unclear. In this study, we investigated the immune microenvironment by multiomics analysis. The tumour immune infiltration characteristics of HCC were determined at the genomic, epigenetic, bulk transcriptome and single-cell levels by data from The Cancer Genome Atlas portal and the Gene Expression Omnibus (GEO). An epigenetic immune-related scoring system (EIRS) was developed to stratify patients with poor prognosis. SPP1, one gene in the EIRS system, was identified as an immune-related predictor of poor survival in HCC patients. Through receptor-ligand pair analysis in single-cell RNA-seq, SPP1 was indicated to mediate the crosstalk between HCC cells and macrophages via SPP1-CD44 and SPP1-PTGER4 association. In vitro experiments further validate SPP1 can trigger the polarization of macrophages to M2-phenotype tumour-associated macrophages (TAMs).</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>34028567</pmid><doi>10.1007/s00262-021-02967-8</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-7066-2937</orcidid><orcidid>https://orcid.org/0000-0002-6232-3783</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Algorithms Cancer Research Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology CD44 antigen Cell Line, Tumor Cell Movement Coculture Techniques Disease-Free Survival DNA Methylation Epigenetics Female Gene expression Genome, Human Hep G2 Cells Hepatocellular carcinoma Humans Immune System Immunology Immunotherapy Ligands Liver cancer Liver Neoplasms - metabolism Liver Neoplasms - pathology Macrophages Macrophages - metabolism Male Medical prognosis Medicine Medicine & Public Health Metastases Microenvironments Middle Aged Monocytes - metabolism Oncology Original Original Article Osteopontin - metabolism Phenotype Phenotypes Prognosis RNA, Small Interfering - metabolism Transcriptomes Treatment Outcome Tumor Microenvironment Tumors |
| title | Construction of TME and Identification of crosstalk between malignant cells and macrophages by SPP1 in hepatocellular carcinoma |
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