ANGPTL8 links inflammation and poor differentiation, which are characteristics of malignant renal cell carcinoma
Inflammation is observed in many tumors, which affects metastasis, infiltration, and immune escape and causes poor differentiation of the cancer cells. However, the molecular basis underlying the relationship between inflammation and poor differentiation in tumors has not been identified. In this st...
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| Veröffentlicht in: | Cancer science 2023-04, Vol.114 (4), p.1410-1422 |
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| creator | Matsukawa, Takuo Doi, Tomomitsu Obayashi, Kunie Sumida, Kazuhiro Fujimoto, Naohiro Endo, Motoyoshi |
| description | Inflammation is observed in many tumors, which affects metastasis, infiltration, and immune escape and causes poor differentiation of the cancer cells. However, the molecular basis underlying the relationship between inflammation and poor differentiation in tumors has not been identified. In this study, we demonstrate that angiopoietin‐like protein‐8 (ANGPTL8), which is induced by stress stimuli such as inflammation, is involved in the maintenance of the undifferentiated state of clear cell renal cell carcinoma (ccRCC) cells. ANGPTL8 is also involved in the production of chemokines that attract immune suppressor cells to the tumor microenvironment. ANGPTL8 sustains the continuous production of chemokines by activating the NF‐κB signaling pathway and maintains the undifferentiated state of ccRCC cells. Finally, ANGPTL8 is induced by STAT3 signaling, which is activated by immune cells in the tumor microenvironment. These results support a role for ANGPTL8 in determining the properties of ccRCC by hampering tumor cell differentiation and establishing the tumor microenvironment.
ANGPTL8 maintains the undifferentiated state in renal carcinoma and upregulates CXCL1 and CXCL2 to attract immune cells, which activates STAT3 signaling for ANGPTL8 induction in the tumor microenvironment. |
| doi_str_mv | 10.1111/cas.15700 |
| format | Article |
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ANGPTL8 maintains the undifferentiated state in renal carcinoma and upregulates CXCL1 and CXCL2 to attract immune cells, which activates STAT3 signaling for ANGPTL8 induction in the tumor microenvironment.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.15700</identifier><identifier>PMID: 36529524</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Angiopoietin ; Angiopoietin-Like Protein 8 - genetics ; angiopoietin‐like protein‐8 ; Antibodies ; Carcinoma, Renal Cell - genetics ; Carcinoma, Renal Cell - pathology ; Cell Differentiation ; Cell growth ; Chemokines ; Clear cell-type renal cell carcinoma ; Cloning ; Genomes ; Humans ; Inflammation ; Kidney cancer ; Kidney Neoplasms - genetics ; Metastases ; NF-κB protein ; Original ; Peptide Hormones - metabolism ; Proteins ; renal cell carcinoma ; Signal transduction ; Stat3 protein ; Suppressor cells ; Tumor Microenvironment ; Tumor necrosis factor-TNF ; undifferentiation</subject><ispartof>Cancer science, 2023-04, Vol.114 (4), p.1410-1422</ispartof><rights>2023 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2023 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2023. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5340-437554177214c168759fbd06301b486059c14b885cddc8ab826d2940e52d7ce43</citedby><cites>FETCH-LOGICAL-c5340-437554177214c168759fbd06301b486059c14b885cddc8ab826d2940e52d7ce43</cites><orcidid>0000-0002-8287-2456</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/PMC10067409/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10067409/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36529524$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsukawa, Takuo</creatorcontrib><creatorcontrib>Doi, Tomomitsu</creatorcontrib><creatorcontrib>Obayashi, Kunie</creatorcontrib><creatorcontrib>Sumida, Kazuhiro</creatorcontrib><creatorcontrib>Fujimoto, Naohiro</creatorcontrib><creatorcontrib>Endo, Motoyoshi</creatorcontrib><title>ANGPTL8 links inflammation and poor differentiation, which are characteristics of malignant renal cell carcinoma</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>Inflammation is observed in many tumors, which affects metastasis, infiltration, and immune escape and causes poor differentiation of the cancer cells. However, the molecular basis underlying the relationship between inflammation and poor differentiation in tumors has not been identified. In this study, we demonstrate that angiopoietin‐like protein‐8 (ANGPTL8), which is induced by stress stimuli such as inflammation, is involved in the maintenance of the undifferentiated state of clear cell renal cell carcinoma (ccRCC) cells. ANGPTL8 is also involved in the production of chemokines that attract immune suppressor cells to the tumor microenvironment. ANGPTL8 sustains the continuous production of chemokines by activating the NF‐κB signaling pathway and maintains the undifferentiated state of ccRCC cells. Finally, ANGPTL8 is induced by STAT3 signaling, which is activated by immune cells in the tumor microenvironment. These results support a role for ANGPTL8 in determining the properties of ccRCC by hampering tumor cell differentiation and establishing the tumor microenvironment.
ANGPTL8 maintains the undifferentiated state in renal carcinoma and upregulates CXCL1 and CXCL2 to attract immune cells, which activates STAT3 signaling for ANGPTL8 induction in the tumor microenvironment.</description><subject>Angiopoietin</subject><subject>Angiopoietin-Like Protein 8 - genetics</subject><subject>angiopoietin‐like protein‐8</subject><subject>Antibodies</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Carcinoma, Renal Cell - pathology</subject><subject>Cell Differentiation</subject><subject>Cell growth</subject><subject>Chemokines</subject><subject>Clear cell-type renal cell carcinoma</subject><subject>Cloning</subject><subject>Genomes</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Kidney cancer</subject><subject>Kidney Neoplasms - genetics</subject><subject>Metastases</subject><subject>NF-κB protein</subject><subject>Original</subject><subject>Peptide Hormones - metabolism</subject><subject>Proteins</subject><subject>renal cell carcinoma</subject><subject>Signal transduction</subject><subject>Stat3 protein</subject><subject>Suppressor cells</subject><subject>Tumor Microenvironment</subject><subject>Tumor necrosis factor-TNF</subject><subject>undifferentiation</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><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>eNp1kU1P3DAQhq2qqHy0h_6BylJPSAT8GcenarXiS1q1SNCzNXEc1jSxt3YWxL_H7AKih_owHmmeeT2eF6GvlBzTck4s5GMqFSEf0B7lQlclrT9uclVpwtku2s_5jhBeCy0-oV1eS6YlE3toNft5fnWzaPDgw5-MfegHGEeYfAwYQodXMSbc-b53yYXJbwpH-GHp7RJDctguIYGdXPJ58jbj2OMRBn8bIEy4tMCArRtKgGR9iCN8Rjs9DNl9ebkP0O-z05v5RbX4dX45ny0qK7kgleBKSkGVYlRYWjdK6r7tSM0JbUVTE6ktFW3TSNt1toG2YXXHtCBOsk5ZJ_gB-rHVXa3b0XW2TJ9gMKvkR0iPJoI3_1aCX5rbeG9o2Z0SRBeF7y8KKf5duzyZu7hO5UfZMKW5KovlrFCHW8qmmHNy_dsTlJhnd0xxx2zcKey39zO9ka92FOBkCzz4wT3-X8nMZ9dbySfTAJm8</recordid><startdate>202304</startdate><enddate>202304</enddate><creator>Matsukawa, Takuo</creator><creator>Doi, Tomomitsu</creator><creator>Obayashi, Kunie</creator><creator>Sumida, Kazuhiro</creator><creator>Fujimoto, Naohiro</creator><creator>Endo, Motoyoshi</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><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>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8287-2456</orcidid></search><sort><creationdate>202304</creationdate><title>ANGPTL8 links inflammation and poor differentiation, which are characteristics of malignant renal cell carcinoma</title><author>Matsukawa, Takuo ; Doi, Tomomitsu ; Obayashi, Kunie ; Sumida, Kazuhiro ; Fujimoto, Naohiro ; Endo, Motoyoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5340-437554177214c168759fbd06301b486059c14b885cddc8ab826d2940e52d7ce43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Angiopoietin</topic><topic>Angiopoietin-Like Protein 8 - genetics</topic><topic>angiopoietin‐like protein‐8</topic><topic>Antibodies</topic><topic>Carcinoma, Renal Cell - genetics</topic><topic>Carcinoma, Renal Cell - pathology</topic><topic>Cell Differentiation</topic><topic>Cell growth</topic><topic>Chemokines</topic><topic>Clear cell-type renal cell carcinoma</topic><topic>Cloning</topic><topic>Genomes</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Kidney cancer</topic><topic>Kidney Neoplasms - genetics</topic><topic>Metastases</topic><topic>NF-κB protein</topic><topic>Original</topic><topic>Peptide Hormones - metabolism</topic><topic>Proteins</topic><topic>renal cell carcinoma</topic><topic>Signal transduction</topic><topic>Stat3 protein</topic><topic>Suppressor cells</topic><topic>Tumor Microenvironment</topic><topic>Tumor necrosis factor-TNF</topic><topic>undifferentiation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsukawa, Takuo</creatorcontrib><creatorcontrib>Doi, Tomomitsu</creatorcontrib><creatorcontrib>Obayashi, Kunie</creatorcontrib><creatorcontrib>Sumida, Kazuhiro</creatorcontrib><creatorcontrib>Fujimoto, Naohiro</creatorcontrib><creatorcontrib>Endo, Motoyoshi</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Access via ProQuest (Open Access)</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>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matsukawa, Takuo</au><au>Doi, Tomomitsu</au><au>Obayashi, Kunie</au><au>Sumida, Kazuhiro</au><au>Fujimoto, Naohiro</au><au>Endo, Motoyoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ANGPTL8 links inflammation and poor differentiation, which are characteristics of malignant renal cell carcinoma</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2023-04</date><risdate>2023</risdate><volume>114</volume><issue>4</issue><spage>1410</spage><epage>1422</epage><pages>1410-1422</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>Inflammation is observed in many tumors, which affects metastasis, infiltration, and immune escape and causes poor differentiation of the cancer cells. However, the molecular basis underlying the relationship between inflammation and poor differentiation in tumors has not been identified. In this study, we demonstrate that angiopoietin‐like protein‐8 (ANGPTL8), which is induced by stress stimuli such as inflammation, is involved in the maintenance of the undifferentiated state of clear cell renal cell carcinoma (ccRCC) cells. ANGPTL8 is also involved in the production of chemokines that attract immune suppressor cells to the tumor microenvironment. ANGPTL8 sustains the continuous production of chemokines by activating the NF‐κB signaling pathway and maintains the undifferentiated state of ccRCC cells. Finally, ANGPTL8 is induced by STAT3 signaling, which is activated by immune cells in the tumor microenvironment. These results support a role for ANGPTL8 in determining the properties of ccRCC by hampering tumor cell differentiation and establishing the tumor microenvironment.
ANGPTL8 maintains the undifferentiated state in renal carcinoma and upregulates CXCL1 and CXCL2 to attract immune cells, which activates STAT3 signaling for ANGPTL8 induction in the tumor microenvironment.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>36529524</pmid><doi>10.1111/cas.15700</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-8287-2456</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Angiopoietin Angiopoietin-Like Protein 8 - genetics angiopoietin‐like protein‐8 Antibodies Carcinoma, Renal Cell - genetics Carcinoma, Renal Cell - pathology Cell Differentiation Cell growth Chemokines Clear cell-type renal cell carcinoma Cloning Genomes Humans Inflammation Kidney cancer Kidney Neoplasms - genetics Metastases NF-κB protein Original Peptide Hormones - metabolism Proteins renal cell carcinoma Signal transduction Stat3 protein Suppressor cells Tumor Microenvironment Tumor necrosis factor-TNF undifferentiation |
| title | ANGPTL8 links inflammation and poor differentiation, which are characteristics of malignant renal cell carcinoma |
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