FBX8 degrades GSTP1 through ubiquitination to suppress colorectal cancer progression
F-box only protein 8 (FBX8), as a critical component of the SKP1-CUL1-F-box (SCF) E3 ubiquitin ligases, has been associated with several malignancies through interacting with a member of proteins. However, the substrates of FBX8 for destruction in the progression of colorectal carcinoma (CRC) need t...
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| Veröffentlicht in: | Cell death & disease 2019-04, Vol.10 (5), p.351, Article 351 |
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| creator | FeiFei, Wang HongHai, Xu YongRong, Yan PingXiang, Wu JianHua, Wu XiaoHui, Zhu JiaoYing, Li JingBo, Sun Kun, Zhou XiaoLi, Ren Lu, Qi XiaoLiang, Lan ZhiQiang, Cheng Na, Tang WenTing, Liao YanQing, Ding Li, Liang |
| description | F-box only protein 8 (FBX8), as a critical component of the SKP1-CUL1-F-box (SCF) E3 ubiquitin ligases, has been associated with several malignancies through interacting with a member of proteins. However, the substrates of FBX8 for destruction in the progression of colorectal carcinoma (CRC) need to be explored. Here, we show that loss of FBX8 accelerates chemical-induced colon tumorigenesis. FBX8 directly targets GSTP1 for ubiquitin-mediated proteasome degradation in CRC. GSTP1 promotes the proliferation, invasion, and metastasis of CRC cells. Furthermore, GSTP1 is upregulated in CRC tissue samples and predicts poor prognosis of CRC patients. The inactivation of FBX8 negatively correlated with increased levels and stability of GSTP1 in clinical CRC tissues and FBX8 knockout transgenic mice. These findings identify a novel ubiquitination pathway as FBX8-GSTP1 axis that regulates the progression of CRC, which might be a potential prognostic biomarker for CRC patients. |
| doi_str_mv | 10.1038/s41419-019-1588-z |
| format | Article |
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However, the substrates of FBX8 for destruction in the progression of colorectal carcinoma (CRC) need to be explored. Here, we show that loss of FBX8 accelerates chemical-induced colon tumorigenesis. FBX8 directly targets GSTP1 for ubiquitin-mediated proteasome degradation in CRC. GSTP1 promotes the proliferation, invasion, and metastasis of CRC cells. Furthermore, GSTP1 is upregulated in CRC tissue samples and predicts poor prognosis of CRC patients. The inactivation of FBX8 negatively correlated with increased levels and stability of GSTP1 in clinical CRC tissues and FBX8 knockout transgenic mice. These findings identify a novel ubiquitination pathway as FBX8-GSTP1 axis that regulates the progression of CRC, which might be a potential prognostic biomarker for CRC patients.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-019-1588-z</identifier><identifier>PMID: 31024008</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/31 ; 13/51 ; 14/19 ; 38/109 ; 631/67/1504/1885 ; 631/80/84/2336 ; 82/51 ; 82/80 ; 96/1 ; Animals ; Antibodies ; Biochemistry ; Biomarkers - metabolism ; Biomedical and Life Sciences ; Cell Biology ; Cell Culture ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - chemically induced ; Colorectal Neoplasms - mortality ; Colorectal Neoplasms - pathology ; Down-Regulation ; F-Box Proteins - antagonists & inhibitors ; F-Box Proteins - genetics ; F-Box Proteins - metabolism ; Glutathione S-Transferase pi - antagonists & inhibitors ; Glutathione S-Transferase pi - genetics ; Glutathione S-Transferase pi - metabolism ; Glutathione transferase ; Humans ; Immunology ; Kaplan-Meier Estimate ; Life Sciences ; Male ; Metastases ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Mice, Transgenic ; Prognosis ; Proteasomes ; RNA Interference ; RNA, Small Interfering - metabolism ; Transgenic mice ; Tumorigenesis ; Ubiquitin ; Ubiquitin-protein ligase ; Ubiquitination</subject><ispartof>Cell death & disease, 2019-04, Vol.10 (5), p.351, Article 351</ispartof><rights>The Author(s) 2019</rights><rights>The Author(s) 2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). 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These findings identify a novel ubiquitination pathway as FBX8-GSTP1 axis that regulates the progression of CRC, which might be a potential prognostic biomarker for CRC patients.</description><subject>13/31</subject><subject>13/51</subject><subject>14/19</subject><subject>38/109</subject><subject>631/67/1504/1885</subject><subject>631/80/84/2336</subject><subject>82/51</subject><subject>82/80</subject><subject>96/1</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Biochemistry</subject><subject>Biomarkers - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - chemically induced</subject><subject>Colorectal Neoplasms - mortality</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Down-Regulation</subject><subject>F-Box Proteins - antagonists & inhibitors</subject><subject>F-Box Proteins - genetics</subject><subject>F-Box Proteins - metabolism</subject><subject>Glutathione S-Transferase pi - antagonists & inhibitors</subject><subject>Glutathione S-Transferase pi - genetics</subject><subject>Glutathione S-Transferase pi - metabolism</subject><subject>Glutathione transferase</subject><subject>Humans</subject><subject>Immunology</subject><subject>Kaplan-Meier Estimate</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Metastases</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Nude</subject><subject>Mice, Transgenic</subject><subject>Prognosis</subject><subject>Proteasomes</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Transgenic mice</subject><subject>Tumorigenesis</subject><subject>Ubiquitin</subject><subject>Ubiquitin-protein ligase</subject><subject>Ubiquitination</subject><issn>2041-4889</issn><issn>2041-4889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</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>eNp1kV9LwzAUxYMoOtQP4IsEfK7e_Gmbvgg6nAqCghN8C2madh21qUkr6Kc3o3POBwMhgfO7597kIHRC4JwAExeeE06yCMImsRDR1w6aUOAk4kJku1v3A3Ts_RLCYgxonOyjA0aAcgAxQfPZ9avAhamcKozHt8_zJ4L7hbNDtcBDXr8PdV-3qq9ti3uL_dB1zniPtW2sM7pXDdaq1cbhztlqJQXyCO2VqvHmeH0eopfZzXx6Fz083t5Prx4iHbOkj1IjCOWsKHmuSiNyTZjOIEuAQpwCyxNKKRQajEpykWZ5XoJWqTLhGaliJGaH6HL07Yb8zRTatL1Tjexc_abcp7Sqln-Vtl7Iyn7IhAsOggaDs7WBs--D8b1c2sG1YWZJKeGZEJSIQJGR0s5670y56UBArrKQYxYyZCFXWcivUHO6Pdqm4ufnA0BHwAeprYz7bf2_6zeBe5Yk</recordid><startdate>20190425</startdate><enddate>20190425</enddate><creator>FeiFei, Wang</creator><creator>HongHai, Xu</creator><creator>YongRong, Yan</creator><creator>PingXiang, Wu</creator><creator>JianHua, Wu</creator><creator>XiaoHui, Zhu</creator><creator>JiaoYing, Li</creator><creator>JingBo, Sun</creator><creator>Kun, Zhou</creator><creator>XiaoLi, Ren</creator><creator>Lu, Qi</creator><creator>XiaoLiang, Lan</creator><creator>ZhiQiang, Cheng</creator><creator>Na, Tang</creator><creator>WenTing, Liao</creator><creator>YanQing, Ding</creator><creator>Li, Liang</creator><general>Nature Publishing Group UK</general><general>Springer Nature B.V</general><scope>C6C</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88I</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>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>20190425</creationdate><title>FBX8 degrades GSTP1 through ubiquitination to suppress colorectal cancer progression</title><author>FeiFei, Wang ; HongHai, Xu ; YongRong, Yan ; PingXiang, Wu ; JianHua, Wu ; XiaoHui, Zhu ; JiaoYing, Li ; JingBo, Sun ; Kun, Zhou ; XiaoLi, Ren ; Lu, Qi ; XiaoLiang, Lan ; ZhiQiang, Cheng ; Na, Tang ; WenTing, Liao ; YanQing, Ding ; Li, Liang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c536t-7e81243df4bafe8bc13c90960205703b62220dc0ea6b879bbf0ca7ae3307a3153</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>13/31</topic><topic>13/51</topic><topic>14/19</topic><topic>38/109</topic><topic>631/67/1504/1885</topic><topic>631/80/84/2336</topic><topic>82/51</topic><topic>82/80</topic><topic>96/1</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Biochemistry</topic><topic>Biomarkers - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Cell Biology</topic><topic>Cell Culture</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - chemically induced</topic><topic>Colorectal Neoplasms - mortality</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Down-Regulation</topic><topic>F-Box Proteins - antagonists & inhibitors</topic><topic>F-Box Proteins - genetics</topic><topic>F-Box Proteins - metabolism</topic><topic>Glutathione S-Transferase pi - antagonists & inhibitors</topic><topic>Glutathione S-Transferase pi - genetics</topic><topic>Glutathione S-Transferase pi - metabolism</topic><topic>Glutathione transferase</topic><topic>Humans</topic><topic>Immunology</topic><topic>Kaplan-Meier Estimate</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Metastases</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Nude</topic><topic>Mice, Transgenic</topic><topic>Prognosis</topic><topic>Proteasomes</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Transgenic mice</topic><topic>Tumorigenesis</topic><topic>Ubiquitin</topic><topic>Ubiquitin-protein ligase</topic><topic>Ubiquitination</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FeiFei, Wang</creatorcontrib><creatorcontrib>HongHai, Xu</creatorcontrib><creatorcontrib>YongRong, Yan</creatorcontrib><creatorcontrib>PingXiang, Wu</creatorcontrib><creatorcontrib>JianHua, Wu</creatorcontrib><creatorcontrib>XiaoHui, Zhu</creatorcontrib><creatorcontrib>JiaoYing, Li</creatorcontrib><creatorcontrib>JingBo, Sun</creatorcontrib><creatorcontrib>Kun, Zhou</creatorcontrib><creatorcontrib>XiaoLi, Ren</creatorcontrib><creatorcontrib>Lu, Qi</creatorcontrib><creatorcontrib>XiaoLiang, Lan</creatorcontrib><creatorcontrib>ZhiQiang, Cheng</creatorcontrib><creatorcontrib>Na, Tang</creatorcontrib><creatorcontrib>WenTing, Liao</creatorcontrib><creatorcontrib>YanQing, Ding</creatorcontrib><creatorcontrib>Li, Liang</creatorcontrib><collection>Springer Nature OA/Free Journals</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 Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</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>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>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content 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>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FeiFei, Wang</au><au>HongHai, Xu</au><au>YongRong, Yan</au><au>PingXiang, Wu</au><au>JianHua, Wu</au><au>XiaoHui, Zhu</au><au>JiaoYing, Li</au><au>JingBo, Sun</au><au>Kun, Zhou</au><au>XiaoLi, Ren</au><au>Lu, Qi</au><au>XiaoLiang, Lan</au><au>ZhiQiang, Cheng</au><au>Na, Tang</au><au>WenTing, Liao</au><au>YanQing, Ding</au><au>Li, Liang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>FBX8 degrades GSTP1 through ubiquitination to suppress colorectal cancer progression</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2019-04-25</date><risdate>2019</risdate><volume>10</volume><issue>5</issue><spage>351</spage><pages>351-</pages><artnum>351</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>F-box only protein 8 (FBX8), as a critical component of the SKP1-CUL1-F-box (SCF) E3 ubiquitin ligases, has been associated with several malignancies through interacting with a member of proteins. However, the substrates of FBX8 for destruction in the progression of colorectal carcinoma (CRC) need to be explored. Here, we show that loss of FBX8 accelerates chemical-induced colon tumorigenesis. FBX8 directly targets GSTP1 for ubiquitin-mediated proteasome degradation in CRC. GSTP1 promotes the proliferation, invasion, and metastasis of CRC cells. Furthermore, GSTP1 is upregulated in CRC tissue samples and predicts poor prognosis of CRC patients. The inactivation of FBX8 negatively correlated with increased levels and stability of GSTP1 in clinical CRC tissues and FBX8 knockout transgenic mice. These findings identify a novel ubiquitination pathway as FBX8-GSTP1 axis that regulates the progression of CRC, which might be a potential prognostic biomarker for CRC patients.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31024008</pmid><doi>10.1038/s41419-019-1588-z</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 13/31 13/51 14/19 38/109 631/67/1504/1885 631/80/84/2336 82/51 82/80 96/1 Animals Antibodies Biochemistry Biomarkers - metabolism Biomedical and Life Sciences Cell Biology Cell Culture Cell Line, Tumor Cell Movement Cell Proliferation Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - chemically induced Colorectal Neoplasms - mortality Colorectal Neoplasms - pathology Down-Regulation F-Box Proteins - antagonists & inhibitors F-Box Proteins - genetics F-Box Proteins - metabolism Glutathione S-Transferase pi - antagonists & inhibitors Glutathione S-Transferase pi - genetics Glutathione S-Transferase pi - metabolism Glutathione transferase Humans Immunology Kaplan-Meier Estimate Life Sciences Male Metastases Mice Mice, Inbred C57BL Mice, Nude Mice, Transgenic Prognosis Proteasomes RNA Interference RNA, Small Interfering - metabolism Transgenic mice Tumorigenesis Ubiquitin Ubiquitin-protein ligase Ubiquitination |
| title | FBX8 degrades GSTP1 through ubiquitination to suppress colorectal cancer progression |
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