cGAS suppresses hepatocellular carcinoma independent of its cGAMP synthase activity
Cyclic GMP–AMP synthase (cGAS) is a key innate immune sensor that recognizes cytosolic DNA to induce immune responses against invading pathogens. The role of cGAS is conventionally recognized as a nucleotidyltransferase to catalyze the synthesis of cGAMP upon recognition of cytosolic DNA, which lead...
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| Veröffentlicht in: | Cell death and differentiation 2024-06, Vol.31 (6), p.722-737 |
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| creator | Ma, Dapeng Yang, Min Sun, Caiyu Cui, Xiuling Xiong, Gaozhong Wang, Qiushi Jing, Weiqiang Chen, Haiqiang Lv, Xiaoting Liu, Shili Li, Tao Zhao, Yunxue Han, Lihui |
| description | Cyclic GMP–AMP synthase (cGAS) is a key innate immune sensor that recognizes cytosolic DNA to induce immune responses against invading pathogens. The role of cGAS is conventionally recognized as a nucleotidyltransferase to catalyze the synthesis of cGAMP upon recognition of cytosolic DNA, which leads to the activation of STING and production of type I/III interferon to fight against the pathogen. However, given that hepatocytes are lack of functional STING expression, it is intriguing to define the role of cGAS in hepatocellular carcinoma (HCC), the liver parenchymal cells derived malignancy. In this study, we revealed that cGAS was significantly downregulated in clinical HCC tissues, and its dysregulation contributed to the progression of HCC. We further identified cGAS as an immune tyrosine inhibitory motif (ITIM) containing protein, and demonstrated that cGAS inhibited the progression of HCC and increased the response of HCC to sorafenib treatment by suppressing PI3K/AKT/mTORC1 pathway in cellular and animal models. Mechanistically, cGAS recruits SH2-containing tyrosine phosphatase 1 (SHP1) via ITIM, and dephosphorylates p85 in phosphatidylinositol 3-kinase (PI3K), which leads to the suppression of AKT-mTORC1 pathway. Thus, cGAS is identified as a novel tumor suppressor in HCC via its function independent of its conventional role as cGAMP synthase, which indicates a novel therapeutic strategy for advanced HCC by modulating cGAS signaling. |
| doi_str_mv | 10.1038/s41418-024-01291-9 |
| format | Article |
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The role of cGAS is conventionally recognized as a nucleotidyltransferase to catalyze the synthesis of cGAMP upon recognition of cytosolic DNA, which leads to the activation of STING and production of type I/III interferon to fight against the pathogen. However, given that hepatocytes are lack of functional STING expression, it is intriguing to define the role of cGAS in hepatocellular carcinoma (HCC), the liver parenchymal cells derived malignancy. In this study, we revealed that cGAS was significantly downregulated in clinical HCC tissues, and its dysregulation contributed to the progression of HCC. We further identified cGAS as an immune tyrosine inhibitory motif (ITIM) containing protein, and demonstrated that cGAS inhibited the progression of HCC and increased the response of HCC to sorafenib treatment by suppressing PI3K/AKT/mTORC1 pathway in cellular and animal models. Mechanistically, cGAS recruits SH2-containing tyrosine phosphatase 1 (SHP1) via ITIM, and dephosphorylates p85 in phosphatidylinositol 3-kinase (PI3K), which leads to the suppression of AKT-mTORC1 pathway. Thus, cGAS is identified as a novel tumor suppressor in HCC via its function independent of its conventional role as cGAMP synthase, which indicates a novel therapeutic strategy for advanced HCC by modulating cGAS signaling.</description><identifier>ISSN: 1350-9047</identifier><identifier>ISSN: 1476-5403</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/s41418-024-01291-9</identifier><identifier>PMID: 38594443</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>1-Phosphatidylinositol 3-kinase ; 13/1 ; 13/109 ; 13/51 ; 13/89 ; 13/95 ; 14/5 ; 14/63 ; 59 ; 64 ; 64/60 ; 692/308/1426 ; 692/699/67/1244 ; AKT protein ; Animal models ; Animals ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; Cell Biology ; Cell Cycle Analysis ; Cell Line, Tumor ; Hepatocellular carcinoma ; Hepatocytes ; Humans ; Immune response ; Kinases ; Life Sciences ; Liver cancer ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Male ; Malignancy ; Mechanistic Target of Rapamycin Complex 1 - metabolism ; Mice ; Mice, Nude ; Nucleotides, Cyclic - metabolism ; Nucleotidyltransferases - metabolism ; Pathogens ; Phosphatidylinositol 3-Kinases - metabolism ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 - metabolism ; Protein-tyrosine-phosphatase ; Proto-Oncogene Proteins c-akt - metabolism ; SHP-1 protein ; Signal Transduction ; Stem Cells ; Tumor suppressor genes</subject><ispartof>Cell death and differentiation, 2024-06, Vol.31 (6), p.722-737</ispartof><rights>The Author(s), under exclusive licence to ADMC Associazione Differenziamento e Morte Cellulare 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. The Author(s), under exclusive licence to ADMC Associazione Differenziamento e Morte Cellulare.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c326t-96cfe8cac4e2ca73a765f4b4d4e339c6beefc0655e72121226491abe04efaf3b3</cites><orcidid>0000-0002-3001-5364 ; 0000-0003-1030-2232</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41418-024-01291-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41418-024-01291-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38594443$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Dapeng</creatorcontrib><creatorcontrib>Yang, Min</creatorcontrib><creatorcontrib>Sun, Caiyu</creatorcontrib><creatorcontrib>Cui, Xiuling</creatorcontrib><creatorcontrib>Xiong, Gaozhong</creatorcontrib><creatorcontrib>Wang, Qiushi</creatorcontrib><creatorcontrib>Jing, Weiqiang</creatorcontrib><creatorcontrib>Chen, Haiqiang</creatorcontrib><creatorcontrib>Lv, Xiaoting</creatorcontrib><creatorcontrib>Liu, Shili</creatorcontrib><creatorcontrib>Li, Tao</creatorcontrib><creatorcontrib>Zhao, Yunxue</creatorcontrib><creatorcontrib>Han, Lihui</creatorcontrib><title>cGAS suppresses hepatocellular carcinoma independent of its cGAMP synthase activity</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><addtitle>Cell Death Differ</addtitle><description>Cyclic GMP–AMP synthase (cGAS) is a key innate immune sensor that recognizes cytosolic DNA to induce immune responses against invading pathogens. The role of cGAS is conventionally recognized as a nucleotidyltransferase to catalyze the synthesis of cGAMP upon recognition of cytosolic DNA, which leads to the activation of STING and production of type I/III interferon to fight against the pathogen. However, given that hepatocytes are lack of functional STING expression, it is intriguing to define the role of cGAS in hepatocellular carcinoma (HCC), the liver parenchymal cells derived malignancy. In this study, we revealed that cGAS was significantly downregulated in clinical HCC tissues, and its dysregulation contributed to the progression of HCC. We further identified cGAS as an immune tyrosine inhibitory motif (ITIM) containing protein, and demonstrated that cGAS inhibited the progression of HCC and increased the response of HCC to sorafenib treatment by suppressing PI3K/AKT/mTORC1 pathway in cellular and animal models. Mechanistically, cGAS recruits SH2-containing tyrosine phosphatase 1 (SHP1) via ITIM, and dephosphorylates p85 in phosphatidylinositol 3-kinase (PI3K), which leads to the suppression of AKT-mTORC1 pathway. Thus, cGAS is identified as a novel tumor suppressor in HCC via its function independent of its conventional role as cGAMP synthase, which indicates a novel therapeutic strategy for advanced HCC by modulating cGAS signaling.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>13/1</subject><subject>13/109</subject><subject>13/51</subject><subject>13/89</subject><subject>13/95</subject><subject>14/5</subject><subject>14/63</subject><subject>59</subject><subject>64</subject><subject>64/60</subject><subject>692/308/1426</subject><subject>692/699/67/1244</subject><subject>AKT protein</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell Biology</subject><subject>Cell Cycle Analysis</subject><subject>Cell Line, Tumor</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatocytes</subject><subject>Humans</subject><subject>Immune response</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - pathology</subject><subject>Male</subject><subject>Malignancy</subject><subject>Mechanistic Target of Rapamycin Complex 1 - metabolism</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Nucleotides, Cyclic - metabolism</subject><subject>Nucleotidyltransferases - metabolism</subject><subject>Pathogens</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Protein Tyrosine Phosphatase, Non-Receptor Type 6 - metabolism</subject><subject>Protein-tyrosine-phosphatase</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>SHP-1 protein</subject><subject>Signal Transduction</subject><subject>Stem Cells</subject><subject>Tumor suppressor genes</subject><issn>1350-9047</issn><issn>1476-5403</issn><issn>1476-5403</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kF1LwzAUhoMobk7_gBcS8Mabar6aLpdj6BQmCtPrkGanrmNra04r7N-buanghQSSQJ73zeEh5Jyza87k8AYVV3yYMKESxoXhiTkgfa4ynaSKycN4lylLDFNZj5wgLhljOjP6mPTkMDVKKdknMz8ZzSh2TRMAEZAuoHFt7WG16lYuUO-CL6t67WhZzaGBuFUtrQtatkhj9vGZ4qZqFw6BOt-WH2W7OSVHhVshnO3PAXm9u30Z3yfTp8nDeDRNvBS6TYz2BQy98wqEd5l0mU4Llau5AimN1zlA4ZlOU8gEj0toZbjLgSkoXCFzOSBXu94m1O8dYGvXJW4ndxXUHVrJZBpNCKYievkHXdZdqOJ0kdKaaylMFimxo3yoEQMUtgnl2oWN5cxuldudchuV2y_l1sTQxb66y9cw_4l8O46A3AEYn6o3CL9__1P7CVF2jIA</recordid><startdate>20240601</startdate><enddate>20240601</enddate><creator>Ma, Dapeng</creator><creator>Yang, Min</creator><creator>Sun, Caiyu</creator><creator>Cui, Xiuling</creator><creator>Xiong, Gaozhong</creator><creator>Wang, Qiushi</creator><creator>Jing, Weiqiang</creator><creator>Chen, Haiqiang</creator><creator>Lv, Xiaoting</creator><creator>Liu, Shili</creator><creator>Li, Tao</creator><creator>Zhao, Yunxue</creator><creator>Han, Lihui</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-3001-5364</orcidid><orcidid>https://orcid.org/0000-0003-1030-2232</orcidid></search><sort><creationdate>20240601</creationdate><title>cGAS suppresses hepatocellular carcinoma independent of its cGAMP synthase activity</title><author>Ma, Dapeng ; 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The role of cGAS is conventionally recognized as a nucleotidyltransferase to catalyze the synthesis of cGAMP upon recognition of cytosolic DNA, which leads to the activation of STING and production of type I/III interferon to fight against the pathogen. However, given that hepatocytes are lack of functional STING expression, it is intriguing to define the role of cGAS in hepatocellular carcinoma (HCC), the liver parenchymal cells derived malignancy. In this study, we revealed that cGAS was significantly downregulated in clinical HCC tissues, and its dysregulation contributed to the progression of HCC. We further identified cGAS as an immune tyrosine inhibitory motif (ITIM) containing protein, and demonstrated that cGAS inhibited the progression of HCC and increased the response of HCC to sorafenib treatment by suppressing PI3K/AKT/mTORC1 pathway in cellular and animal models. Mechanistically, cGAS recruits SH2-containing tyrosine phosphatase 1 (SHP1) via ITIM, and dephosphorylates p85 in phosphatidylinositol 3-kinase (PI3K), which leads to the suppression of AKT-mTORC1 pathway. Thus, cGAS is identified as a novel tumor suppressor in HCC via its function independent of its conventional role as cGAMP synthase, which indicates a novel therapeutic strategy for advanced HCC by modulating cGAS signaling.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>38594443</pmid><doi>10.1038/s41418-024-01291-9</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-3001-5364</orcidid><orcidid>https://orcid.org/0000-0003-1030-2232</orcidid></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase 13/1 13/109 13/51 13/89 13/95 14/5 14/63 59 64 64/60 692/308/1426 692/699/67/1244 AKT protein Animal models Animals Apoptosis Biochemistry Biomedical and Life Sciences Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology Cell Biology Cell Cycle Analysis Cell Line, Tumor Hepatocellular carcinoma Hepatocytes Humans Immune response Kinases Life Sciences Liver cancer Liver Neoplasms - metabolism Liver Neoplasms - pathology Male Malignancy Mechanistic Target of Rapamycin Complex 1 - metabolism Mice Mice, Nude Nucleotides, Cyclic - metabolism Nucleotidyltransferases - metabolism Pathogens Phosphatidylinositol 3-Kinases - metabolism Protein Tyrosine Phosphatase, Non-Receptor Type 6 - metabolism Protein-tyrosine-phosphatase Proto-Oncogene Proteins c-akt - metabolism SHP-1 protein Signal Transduction Stem Cells Tumor suppressor genes |
| title | cGAS suppresses hepatocellular carcinoma independent of its cGAMP synthase activity |
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