Peptostreptococcus stomatis promotes colonic tumorigenesis and receptor tyrosine kinase inhibitor resistance by activating ERBB2-MAPK
Peptostreptococcus stomatis (P. stomatis) is enriched in colorectal cancer (CRC), but its causality and translational implications in CRC are unknown. Here, we show that P. stomatis accelerates colonic tumorigenesis in ApcMin/+ and azoxymethane/dextran sodium sulfate (AOM-DSS) models by inducing cel...
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| Veröffentlicht in: | Cell host & microbe 2024-08, Vol.32 (8), p.1365-1379.e10 |
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| creator | Huang, Pingmei Ji, Fenfen Cheung, Alvin Ho-Kwan Fu, Kaili Zhou, Qiming Ding, Xiao Chen, Danyu Lin, Yufeng Wang, Luyao Jiao, Ying Chu, Eagle S.H. Kang, Wei To, Ka Fai Yu, Jun Wong, Chi Chun |
| description | Peptostreptococcus stomatis (P. stomatis) is enriched in colorectal cancer (CRC), but its causality and translational implications in CRC are unknown. Here, we show that P. stomatis accelerates colonic tumorigenesis in ApcMin/+ and azoxymethane/dextran sodium sulfate (AOM-DSS) models by inducing cell proliferation, suppressing apoptosis, and impairing gut barrier function. P. stomatis adheres to CRC cells through its surface protein fructose-1,6-bisphosphate aldolase (FBA) that binds to the integrin α6/β4 receptor on CRC cells, leading to the activation of ERBB2 and the downstream MEK-ERK-p90 cascade. Blockade of the FBA-integrin α6/β4 abolishes ERBB2-mitogen-activated protein kinase (MAPK) activation and the protumorigenic effect of P. stomatis. P. stomatis-driven ERBB2 activation bypasses receptor tyrosine kinase (RTK) blockade by EGFR inhibitors (cetuximab, erlotinib), leading to drug resistance in xenograft and spontaneous CRC models of KRAS-wild-type CRC. P. stomatis also abrogates BRAF inhibitor (vemurafenib) efficacy in BRAFV600E-mutant CRC xenografts. Thus, we identify P. stomatis as an oncogenic bacterium and a contributory factor for non-responsiveness to RTK inhibitors in CRC.
[Display omitted]
•P. stomatis is enriched in CRC patients and promotes colorectal tumorigenesis in mice•P. stomatis attaches to CRC cells via binding of its adhesin FBA to integrin α6/β4•P. stomatis induces ERBB2-MEK-ERK-p90 cascade to promote tumorigenesis•P. stomatis-driven ERBB2 activation abrogates RTK inhibitor efficacy in CRC
Huang et al. identify a CRC-enriched bacterium, Peptostreptococcus stomatis, that promotes colorectal tumorigenesis. P. stomatis directly interacts with CRC cells via binding of its adhesin FBA to the host integrin α6/β4, leading to ERBB2-MAPK activation. P. stomatis-mediated ERBB2-MAPK signaling contributes to resistance to multiple receptor tyrosine kinase inhibitors in CRC. |
| doi_str_mv | 10.1016/j.chom.2024.07.001 |
| format | Article |
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[Display omitted]
•P. stomatis is enriched in CRC patients and promotes colorectal tumorigenesis in mice•P. stomatis attaches to CRC cells via binding of its adhesin FBA to integrin α6/β4•P. stomatis induces ERBB2-MEK-ERK-p90 cascade to promote tumorigenesis•P. stomatis-driven ERBB2 activation abrogates RTK inhibitor efficacy in CRC
Huang et al. identify a CRC-enriched bacterium, Peptostreptococcus stomatis, that promotes colorectal tumorigenesis. P. stomatis directly interacts with CRC cells via binding of its adhesin FBA to the host integrin α6/β4, leading to ERBB2-MAPK activation. P. stomatis-mediated ERBB2-MAPK signaling contributes to resistance to multiple receptor tyrosine kinase inhibitors in CRC.</description><identifier>ISSN: 1931-3128</identifier><identifier>ISSN: 1934-6069</identifier><identifier>EISSN: 1934-6069</identifier><identifier>DOI: 10.1016/j.chom.2024.07.001</identifier><identifier>PMID: 39059397</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Apoptosis - drug effects ; Carcinogenesis ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Colonic Neoplasms ; colorectal cancer ; Colorectal Neoplasms ; drug resistance ; Drug Resistance, Neoplasm ; Fructose-Bisphosphate Aldolase - genetics ; Fructose-Bisphosphate Aldolase - metabolism ; host-microbe interaction ; Humans ; MAP Kinase Signaling System - drug effects ; Mice ; Mitogen-Activated Protein Kinases - genetics ; Mitogen-Activated Protein Kinases - metabolism ; Peptostreptococcus ; Peptostreptococcus Stomatis ; Protein Kinase Inhibitors - pharmacology ; receptor tyrosine kinase inhibitor ; Receptor, ErbB-2 - genetics ; Receptor, ErbB-2 - metabolism ; Tyrosine Kinase Inhibitors</subject><ispartof>Cell host & microbe, 2024-08, Vol.32 (8), p.1365-1379.e10</ispartof><rights>2024 The Author(s)</rights><rights>Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c281t-b3e0581f4eaeeb9b78279f8366b1d214e4d8a0ed9719d78632c2822606e696723</cites><orcidid>0000-0001-5008-2153</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.chom.2024.07.001$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39059397$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Pingmei</creatorcontrib><creatorcontrib>Ji, Fenfen</creatorcontrib><creatorcontrib>Cheung, Alvin Ho-Kwan</creatorcontrib><creatorcontrib>Fu, Kaili</creatorcontrib><creatorcontrib>Zhou, Qiming</creatorcontrib><creatorcontrib>Ding, Xiao</creatorcontrib><creatorcontrib>Chen, Danyu</creatorcontrib><creatorcontrib>Lin, Yufeng</creatorcontrib><creatorcontrib>Wang, Luyao</creatorcontrib><creatorcontrib>Jiao, Ying</creatorcontrib><creatorcontrib>Chu, Eagle S.H.</creatorcontrib><creatorcontrib>Kang, Wei</creatorcontrib><creatorcontrib>To, Ka Fai</creatorcontrib><creatorcontrib>Yu, Jun</creatorcontrib><creatorcontrib>Wong, Chi Chun</creatorcontrib><title>Peptostreptococcus stomatis promotes colonic tumorigenesis and receptor tyrosine kinase inhibitor resistance by activating ERBB2-MAPK</title><title>Cell host & microbe</title><addtitle>Cell Host Microbe</addtitle><description>Peptostreptococcus stomatis (P. stomatis) is enriched in colorectal cancer (CRC), but its causality and translational implications in CRC are unknown. Here, we show that P. stomatis accelerates colonic tumorigenesis in ApcMin/+ and azoxymethane/dextran sodium sulfate (AOM-DSS) models by inducing cell proliferation, suppressing apoptosis, and impairing gut barrier function. P. stomatis adheres to CRC cells through its surface protein fructose-1,6-bisphosphate aldolase (FBA) that binds to the integrin α6/β4 receptor on CRC cells, leading to the activation of ERBB2 and the downstream MEK-ERK-p90 cascade. Blockade of the FBA-integrin α6/β4 abolishes ERBB2-mitogen-activated protein kinase (MAPK) activation and the protumorigenic effect of P. stomatis. P. stomatis-driven ERBB2 activation bypasses receptor tyrosine kinase (RTK) blockade by EGFR inhibitors (cetuximab, erlotinib), leading to drug resistance in xenograft and spontaneous CRC models of KRAS-wild-type CRC. P. stomatis also abrogates BRAF inhibitor (vemurafenib) efficacy in BRAFV600E-mutant CRC xenografts. Thus, we identify P. stomatis as an oncogenic bacterium and a contributory factor for non-responsiveness to RTK inhibitors in CRC.
[Display omitted]
•P. stomatis is enriched in CRC patients and promotes colorectal tumorigenesis in mice•P. stomatis attaches to CRC cells via binding of its adhesin FBA to integrin α6/β4•P. stomatis induces ERBB2-MEK-ERK-p90 cascade to promote tumorigenesis•P. stomatis-driven ERBB2 activation abrogates RTK inhibitor efficacy in CRC
Huang et al. identify a CRC-enriched bacterium, Peptostreptococcus stomatis, that promotes colorectal tumorigenesis. P. stomatis directly interacts with CRC cells via binding of its adhesin FBA to the host integrin α6/β4, leading to ERBB2-MAPK activation. P. stomatis-mediated ERBB2-MAPK signaling contributes to resistance to multiple receptor tyrosine kinase inhibitors in CRC.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Carcinogenesis</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Colonic Neoplasms</subject><subject>colorectal cancer</subject><subject>Colorectal Neoplasms</subject><subject>drug resistance</subject><subject>Drug Resistance, Neoplasm</subject><subject>Fructose-Bisphosphate Aldolase - genetics</subject><subject>Fructose-Bisphosphate Aldolase - metabolism</subject><subject>host-microbe interaction</subject><subject>Humans</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Mice</subject><subject>Mitogen-Activated Protein Kinases - genetics</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Peptostreptococcus</subject><subject>Peptostreptococcus Stomatis</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>receptor tyrosine kinase inhibitor</subject><subject>Receptor, ErbB-2 - genetics</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>Tyrosine Kinase Inhibitors</subject><issn>1931-3128</issn><issn>1934-6069</issn><issn>1934-6069</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM1O3DAUha2KqlDoC7BAXrJJ8E9ix1I3MIKCoCpC7dpynDvgYWJPbQdpHqDvjdOBLrs6V7rnHOl8CB1TUlNCxdmqtk9hrBlhTU1kTQj9gA6o4k0liFB7f29accq6ffQ5pRUhbUsk_YT2uSKt4koeoD_3sMkh5TiLDdZOCaccRpNdwpsYxpAhYRvWwTuL8zSG6B7BQypv4wccwc7JiPM2huQ84GfnTQLs_JPr3fyJszkbbwH3W2xsdi-l3T_iy4eLC1Z9P7-_PUIfl2ad4MubHqJfV5c_F9fV3Y9vN4vzu8qyjuaq50Daji4bMAC96mXHpFp2XIieDow20AydITAoSdUgO8FZyTFWaIBQQjJ-iE53vWXZ7wlS1qNLFtZr4yFMSXPStZQKyWcr21lt2ZUiLPUmutHEraZEz_j1Ss_49YxfE6kL_hI6eeuf-hGGf5F33sXwdWeAsvLFQdTJOihoBldIZj0E97_-V5p4mQ4</recordid><startdate>20240814</startdate><enddate>20240814</enddate><creator>Huang, Pingmei</creator><creator>Ji, Fenfen</creator><creator>Cheung, Alvin Ho-Kwan</creator><creator>Fu, Kaili</creator><creator>Zhou, Qiming</creator><creator>Ding, Xiao</creator><creator>Chen, Danyu</creator><creator>Lin, Yufeng</creator><creator>Wang, Luyao</creator><creator>Jiao, Ying</creator><creator>Chu, Eagle S.H.</creator><creator>Kang, Wei</creator><creator>To, Ka Fai</creator><creator>Yu, Jun</creator><creator>Wong, Chi Chun</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope><orcidid>https://orcid.org/0000-0001-5008-2153</orcidid></search><sort><creationdate>20240814</creationdate><title>Peptostreptococcus stomatis promotes colonic tumorigenesis and receptor tyrosine kinase inhibitor resistance by activating ERBB2-MAPK</title><author>Huang, Pingmei ; Ji, Fenfen ; Cheung, Alvin Ho-Kwan ; Fu, Kaili ; Zhou, Qiming ; Ding, Xiao ; Chen, Danyu ; Lin, Yufeng ; Wang, Luyao ; Jiao, Ying ; Chu, Eagle S.H. ; Kang, Wei ; To, Ka Fai ; Yu, Jun ; Wong, Chi Chun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c281t-b3e0581f4eaeeb9b78279f8366b1d214e4d8a0ed9719d78632c2822606e696723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Carcinogenesis</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Colonic Neoplasms</topic><topic>colorectal cancer</topic><topic>Colorectal Neoplasms</topic><topic>drug resistance</topic><topic>Drug Resistance, Neoplasm</topic><topic>Fructose-Bisphosphate Aldolase - genetics</topic><topic>Fructose-Bisphosphate Aldolase - metabolism</topic><topic>host-microbe interaction</topic><topic>Humans</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Mice</topic><topic>Mitogen-Activated Protein Kinases - genetics</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Peptostreptococcus</topic><topic>Peptostreptococcus Stomatis</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>receptor tyrosine kinase inhibitor</topic><topic>Receptor, ErbB-2 - genetics</topic><topic>Receptor, ErbB-2 - metabolism</topic><topic>Tyrosine Kinase Inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Pingmei</creatorcontrib><creatorcontrib>Ji, Fenfen</creatorcontrib><creatorcontrib>Cheung, Alvin Ho-Kwan</creatorcontrib><creatorcontrib>Fu, Kaili</creatorcontrib><creatorcontrib>Zhou, Qiming</creatorcontrib><creatorcontrib>Ding, Xiao</creatorcontrib><creatorcontrib>Chen, Danyu</creatorcontrib><creatorcontrib>Lin, Yufeng</creatorcontrib><creatorcontrib>Wang, Luyao</creatorcontrib><creatorcontrib>Jiao, Ying</creatorcontrib><creatorcontrib>Chu, Eagle S.H.</creatorcontrib><creatorcontrib>Kang, Wei</creatorcontrib><creatorcontrib>To, Ka Fai</creatorcontrib><creatorcontrib>Yu, Jun</creatorcontrib><creatorcontrib>Wong, Chi Chun</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cell host & microbe</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Pingmei</au><au>Ji, Fenfen</au><au>Cheung, Alvin Ho-Kwan</au><au>Fu, Kaili</au><au>Zhou, Qiming</au><au>Ding, Xiao</au><au>Chen, Danyu</au><au>Lin, Yufeng</au><au>Wang, Luyao</au><au>Jiao, Ying</au><au>Chu, Eagle S.H.</au><au>Kang, Wei</au><au>To, Ka Fai</au><au>Yu, Jun</au><au>Wong, Chi Chun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peptostreptococcus stomatis promotes colonic tumorigenesis and receptor tyrosine kinase inhibitor resistance by activating ERBB2-MAPK</atitle><jtitle>Cell host & microbe</jtitle><addtitle>Cell Host Microbe</addtitle><date>2024-08-14</date><risdate>2024</risdate><volume>32</volume><issue>8</issue><spage>1365</spage><epage>1379.e10</epage><pages>1365-1379.e10</pages><issn>1931-3128</issn><issn>1934-6069</issn><eissn>1934-6069</eissn><abstract>Peptostreptococcus stomatis (P. stomatis) is enriched in colorectal cancer (CRC), but its causality and translational implications in CRC are unknown. Here, we show that P. stomatis accelerates colonic tumorigenesis in ApcMin/+ and azoxymethane/dextran sodium sulfate (AOM-DSS) models by inducing cell proliferation, suppressing apoptosis, and impairing gut barrier function. P. stomatis adheres to CRC cells through its surface protein fructose-1,6-bisphosphate aldolase (FBA) that binds to the integrin α6/β4 receptor on CRC cells, leading to the activation of ERBB2 and the downstream MEK-ERK-p90 cascade. Blockade of the FBA-integrin α6/β4 abolishes ERBB2-mitogen-activated protein kinase (MAPK) activation and the protumorigenic effect of P. stomatis. P. stomatis-driven ERBB2 activation bypasses receptor tyrosine kinase (RTK) blockade by EGFR inhibitors (cetuximab, erlotinib), leading to drug resistance in xenograft and spontaneous CRC models of KRAS-wild-type CRC. P. stomatis also abrogates BRAF inhibitor (vemurafenib) efficacy in BRAFV600E-mutant CRC xenografts. Thus, we identify P. stomatis as an oncogenic bacterium and a contributory factor for non-responsiveness to RTK inhibitors in CRC.
[Display omitted]
•P. stomatis is enriched in CRC patients and promotes colorectal tumorigenesis in mice•P. stomatis attaches to CRC cells via binding of its adhesin FBA to integrin α6/β4•P. stomatis induces ERBB2-MEK-ERK-p90 cascade to promote tumorigenesis•P. stomatis-driven ERBB2 activation abrogates RTK inhibitor efficacy in CRC
Huang et al. identify a CRC-enriched bacterium, Peptostreptococcus stomatis, that promotes colorectal tumorigenesis. P. stomatis directly interacts with CRC cells via binding of its adhesin FBA to the host integrin α6/β4, leading to ERBB2-MAPK activation. P. stomatis-mediated ERBB2-MAPK signaling contributes to resistance to multiple receptor tyrosine kinase inhibitors in CRC.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>39059397</pmid><doi>10.1016/j.chom.2024.07.001</doi><orcidid>https://orcid.org/0000-0001-5008-2153</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis - drug effects Carcinogenesis Cell Line, Tumor Cell Proliferation - drug effects Colonic Neoplasms colorectal cancer Colorectal Neoplasms drug resistance Drug Resistance, Neoplasm Fructose-Bisphosphate Aldolase - genetics Fructose-Bisphosphate Aldolase - metabolism host-microbe interaction Humans MAP Kinase Signaling System - drug effects Mice Mitogen-Activated Protein Kinases - genetics Mitogen-Activated Protein Kinases - metabolism Peptostreptococcus Peptostreptococcus Stomatis Protein Kinase Inhibitors - pharmacology receptor tyrosine kinase inhibitor Receptor, ErbB-2 - genetics Receptor, ErbB-2 - metabolism Tyrosine Kinase Inhibitors |
| title | Peptostreptococcus stomatis promotes colonic tumorigenesis and receptor tyrosine kinase inhibitor resistance by activating ERBB2-MAPK |
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