Autophagic and tumour suppressor activity of a novel Beclin1-binding protein UVRAG
Autophagy, the degradation of cytoplasmic components, is an evolutionarily conserved homeostatic process involved in environmental adaptation, lifespan determination and tumour development. The tumor suppressor Beclin1 is part of the PI(3) kinase class III (PI(3)KC3) lipid-kinase complex that induce...
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| Veröffentlicht in: | Nature cell biology 2006-07, Vol.8 (7), p.688-698 |
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| creator | Liang, Chengyu Feng, Pinghui Ku, Bonsu Dotan, Iris Canaani, Dan Oh, Byung-Ha Jung, Jae U. |
| description | Autophagy, the degradation of cytoplasmic components, is an evolutionarily conserved homeostatic process involved in environmental adaptation, lifespan determination and tumour development. The tumor suppressor Beclin1 is part of the PI(3) kinase class III (PI(3)KC3) lipid-kinase complex that induces autophagy. The autophagic activity of the Beclin1–PI(3)KC3 complex, however, is suppressed by Bcl-2. Here, we report the identification of a novel coiled–coil UV irradiation resistance-associated gene (UVRAG) as a positive regulator of the Beclin1–PI(3)KC3 complex. UVRAG, a tumour suppressor candidate that is monoallelically mutated at high frequency in human colon cancers, associates with the Beclin1–Bcl-2–PI(3)KC3 multiprotein complex, where UVRAG and Beclin1 interdependently induce autophagy. UVRAG-mediated activation of the Beclin1–PI(3)KC3 complex promotes autophagy and also suppresses the proliferation and tumorigenicity of human colon cancer cells. These results identify UVRAG as an essential component of the Beclin1–PI(3)KC3 lipid kinase complex that is an important signalling checkpoint for autophagy and tumour-cell growth. |
| doi_str_mv | 10.1038/ncb1426 |
| format | Article |
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The tumor suppressor Beclin1 is part of the PI(3) kinase class III (PI(3)KC3) lipid-kinase complex that induces autophagy. The autophagic activity of the Beclin1–PI(3)KC3 complex, however, is suppressed by Bcl-2. Here, we report the identification of a novel coiled–coil UV irradiation resistance-associated gene (UVRAG) as a positive regulator of the Beclin1–PI(3)KC3 complex. UVRAG, a tumour suppressor candidate that is monoallelically mutated at high frequency in human colon cancers, associates with the Beclin1–Bcl-2–PI(3)KC3 multiprotein complex, where UVRAG and Beclin1 interdependently induce autophagy. UVRAG-mediated activation of the Beclin1–PI(3)KC3 complex promotes autophagy and also suppresses the proliferation and tumorigenicity of human colon cancer cells. These results identify UVRAG as an essential component of the Beclin1–PI(3)KC3 lipid kinase complex that is an important signalling checkpoint for autophagy and tumour-cell growth.</description><identifier>ISSN: 1465-7392</identifier><identifier>ISSN: 1476-4679</identifier><identifier>EISSN: 1476-4679</identifier><identifier>DOI: 10.1038/ncb1426</identifier><identifier>PMID: 16799551</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animals ; Apoptosis ; Apoptosis - physiology ; Apoptosis Regulatory Proteins ; Autophagy ; Autophagy - physiology ; Beclin-1 ; Binding proteins ; Biomedical and Life Sciences ; Cancer Research ; Carcinoma - genetics ; Carcinoma - metabolism ; Carcinoma - physiopathology ; Cell Biology ; Cell Line, Tumor ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Chromosomes, Human, Pair 11 - genetics ; Colonic Neoplasms - genetics ; Colonic Neoplasms - metabolism ; Colonic Neoplasms - physiopathology ; Colorectal cancer ; Developmental Biology ; Genes ; Genetic aspects ; Herpes viruses ; Humans ; Irradiation ; Kinases ; Life Sciences ; Life span ; Macromolecular Substances - metabolism ; Mice ; Neoplasm Transplantation ; NIH 3T3 Cells ; Phagocytosis ; Physiological aspects ; Protein Binding - physiology ; Proteins ; Proteins - metabolism ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Signal Transduction - physiology ; Stem Cells ; Tumor suppressor genes ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - isolation & purification ; Tumor Suppressor Proteins - metabolism ; Tumors ; Ultraviolet radiation</subject><ispartof>Nature cell biology, 2006-07, Vol.8 (7), p.688-698</ispartof><rights>Springer Nature Limited 2006</rights><rights>COPYRIGHT 2006 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jul 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-4e726cfb757313c157208978e791413603c0a74cf9f1c82ba6e40bd4bf9566013</citedby><cites>FETCH-LOGICAL-c503t-4e726cfb757313c157208978e791413603c0a74cf9f1c82ba6e40bd4bf9566013</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ncb1426$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ncb1426$$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/16799551$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liang, Chengyu</creatorcontrib><creatorcontrib>Feng, Pinghui</creatorcontrib><creatorcontrib>Ku, Bonsu</creatorcontrib><creatorcontrib>Dotan, Iris</creatorcontrib><creatorcontrib>Canaani, Dan</creatorcontrib><creatorcontrib>Oh, Byung-Ha</creatorcontrib><creatorcontrib>Jung, Jae U.</creatorcontrib><title>Autophagic and tumour suppressor activity of a novel Beclin1-binding protein UVRAG</title><title>Nature cell biology</title><addtitle>Nat Cell Biol</addtitle><addtitle>Nat Cell Biol</addtitle><description>Autophagy, the degradation of cytoplasmic components, is an evolutionarily conserved homeostatic process involved in environmental adaptation, lifespan determination and tumour development. The tumor suppressor Beclin1 is part of the PI(3) kinase class III (PI(3)KC3) lipid-kinase complex that induces autophagy. The autophagic activity of the Beclin1–PI(3)KC3 complex, however, is suppressed by Bcl-2. Here, we report the identification of a novel coiled–coil UV irradiation resistance-associated gene (UVRAG) as a positive regulator of the Beclin1–PI(3)KC3 complex. UVRAG, a tumour suppressor candidate that is monoallelically mutated at high frequency in human colon cancers, associates with the Beclin1–Bcl-2–PI(3)KC3 multiprotein complex, where UVRAG and Beclin1 interdependently induce autophagy. UVRAG-mediated activation of the Beclin1–PI(3)KC3 complex promotes autophagy and also suppresses the proliferation and tumorigenicity of human colon cancer cells. These results identify UVRAG as an essential component of the Beclin1–PI(3)KC3 lipid kinase complex that is an important signalling checkpoint for autophagy and tumour-cell growth.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Apoptosis Regulatory Proteins</subject><subject>Autophagy</subject><subject>Autophagy - physiology</subject><subject>Beclin-1</subject><subject>Binding proteins</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer Research</subject><subject>Carcinoma - genetics</subject><subject>Carcinoma - metabolism</subject><subject>Carcinoma - physiopathology</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Chromosomes, Human, Pair 11 - genetics</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colonic Neoplasms - physiopathology</subject><subject>Colorectal cancer</subject><subject>Developmental Biology</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Herpes viruses</subject><subject>Humans</subject><subject>Irradiation</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Life span</subject><subject>Macromolecular Substances - metabolism</subject><subject>Mice</subject><subject>Neoplasm Transplantation</subject><subject>NIH 3T3 Cells</subject><subject>Phagocytosis</subject><subject>Physiological aspects</subject><subject>Protein Binding - physiology</subject><subject>Proteins</subject><subject>Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Signal Transduction - physiology</subject><subject>Stem Cells</subject><subject>Tumor suppressor genes</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumor Suppressor Proteins - isolation & purification</subject><subject>Tumor Suppressor Proteins - metabolism</subject><subject>Tumors</subject><subject>Ultraviolet radiation</subject><issn>1465-7392</issn><issn>1476-4679</issn><issn>1476-4679</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqF0t1r1TAUAPAiiptT_A8kKPjx0Jk0n328Dp2DgXB1voY0TWpGm3RJOtx_by63MO4QTR4Skl_O4YRTVS8RPEUQi49ed4g07FF1jAhnNWG8fbzbM1pz3DZH1bOUriFEhED-tDpC5b6lFB1X282Sw_xLDU4D5XuQlyksEaRlnqNJKUSgdHa3Lt-BYIECPtyaEXwyenQe1Z3zvfMDmGPIxnlw9XO7OX9ePbFqTObFup5UV18-_zj7Wl9-O78421zWmkKca2J4w7TtOOUYYY0ob6BouTC8RQRhBrGGihNtW4u0aDrFDIFdTzrbUsYgwifVu33ckv1mMSnLySVtxlF5E5YkBSwJSpWiyLf_lEywYtvmvxDxhghKdrlfP4DX5dt8KVc2ZQguBCvozR4NajTSeRtyVHoXUW6QwJAKQWhRp39RZfZmcjp4Y105P3jw4eBBMdn8zoNaUpIX37eHdv0jHUNK0Vg5RzepeCcRlLvOkWvnFPlqrWjpJtPfu7VVCni_B6lc-cHE-5IfxvoDCxvGdw</recordid><startdate>20060701</startdate><enddate>20060701</enddate><creator>Liang, Chengyu</creator><creator>Feng, Pinghui</creator><creator>Ku, Bonsu</creator><creator>Dotan, Iris</creator><creator>Canaani, Dan</creator><creator>Oh, Byung-Ha</creator><creator>Jung, Jae U.</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>ISR</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20060701</creationdate><title>Autophagic and tumour suppressor activity of a novel Beclin1-binding protein UVRAG</title><author>Liang, Chengyu ; Feng, Pinghui ; Ku, Bonsu ; Dotan, Iris ; Canaani, Dan ; Oh, Byung-Ha ; Jung, Jae U.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-4e726cfb757313c157208978e791413603c0a74cf9f1c82ba6e40bd4bf9566013</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - 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Academic</collection><jtitle>Nature cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liang, Chengyu</au><au>Feng, Pinghui</au><au>Ku, Bonsu</au><au>Dotan, Iris</au><au>Canaani, Dan</au><au>Oh, Byung-Ha</au><au>Jung, Jae U.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autophagic and tumour suppressor activity of a novel Beclin1-binding protein UVRAG</atitle><jtitle>Nature cell biology</jtitle><stitle>Nat Cell Biol</stitle><addtitle>Nat Cell Biol</addtitle><date>2006-07-01</date><risdate>2006</risdate><volume>8</volume><issue>7</issue><spage>688</spage><epage>698</epage><pages>688-698</pages><issn>1465-7392</issn><issn>1476-4679</issn><eissn>1476-4679</eissn><abstract>Autophagy, the degradation of cytoplasmic components, is an evolutionarily conserved homeostatic process involved in environmental adaptation, lifespan determination and tumour development. The tumor suppressor Beclin1 is part of the PI(3) kinase class III (PI(3)KC3) lipid-kinase complex that induces autophagy. The autophagic activity of the Beclin1–PI(3)KC3 complex, however, is suppressed by Bcl-2. Here, we report the identification of a novel coiled–coil UV irradiation resistance-associated gene (UVRAG) as a positive regulator of the Beclin1–PI(3)KC3 complex. UVRAG, a tumour suppressor candidate that is monoallelically mutated at high frequency in human colon cancers, associates with the Beclin1–Bcl-2–PI(3)KC3 multiprotein complex, where UVRAG and Beclin1 interdependently induce autophagy. UVRAG-mediated activation of the Beclin1–PI(3)KC3 complex promotes autophagy and also suppresses the proliferation and tumorigenicity of human colon cancer cells. These results identify UVRAG as an essential component of the Beclin1–PI(3)KC3 lipid kinase complex that is an important signalling checkpoint for autophagy and tumour-cell growth.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>16799551</pmid><doi>10.1038/ncb1426</doi><tpages>11</tpages></addata></record> |
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| ispartof | Nature cell biology, 2006-07, Vol.8 (7), p.688-698 |
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| subjects | Animals Apoptosis Apoptosis - physiology Apoptosis Regulatory Proteins Autophagy Autophagy - physiology Beclin-1 Binding proteins Biomedical and Life Sciences Cancer Research Carcinoma - genetics Carcinoma - metabolism Carcinoma - physiopathology Cell Biology Cell Line, Tumor Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Chromosomes, Human, Pair 11 - genetics Colonic Neoplasms - genetics Colonic Neoplasms - metabolism Colonic Neoplasms - physiopathology Colorectal cancer Developmental Biology Genes Genetic aspects Herpes viruses Humans Irradiation Kinases Life Sciences Life span Macromolecular Substances - metabolism Mice Neoplasm Transplantation NIH 3T3 Cells Phagocytosis Physiological aspects Protein Binding - physiology Proteins Proteins - metabolism Proto-Oncogene Proteins c-bcl-2 - genetics Proto-Oncogene Proteins c-bcl-2 - metabolism Signal Transduction - physiology Stem Cells Tumor suppressor genes Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - isolation & purification Tumor Suppressor Proteins - metabolism Tumors Ultraviolet radiation |
| title | Autophagic and tumour suppressor activity of a novel Beclin1-binding protein UVRAG |
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