Deubiquitinase USP18 Loss Mislocalizes and Destabilizes KRAS in Lung Cancer
is frequently mutated in lung cancers and is associated with aggressive biology and chemotherapy resistance. Therefore, innovative approaches are needed to treat these lung cancers. Prior work implicated the IFN-stimulated gene 15 (ISG15) deubiquitinase (DUB) USP18 as having antineoplastic activity...
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| Veröffentlicht in: | Molecular cancer research 2017-07, Vol.15 (7), p.905-914 |
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| creator | Mustachio, Lisa Maria Lu, Yun Tafe, Laura J Memoli, Vincent Rodriguez-Canales, Jaime Mino, Barbara Villalobos, Pamela Andrea Wistuba, Ignacio Katayama, Hiroyuki Hanash, Samir M Roszik, Jason Kawakami, Masanori Cho, Kwang-Jin Hancock, John F Chinyengetere, Fadzai Hu, Shanhu Liu, Xi Freemantle, Sarah J Dmitrovsky, Ethan |
| description | is frequently mutated in lung cancers and is associated with aggressive biology and chemotherapy resistance. Therefore, innovative approaches are needed to treat these lung cancers. Prior work implicated the IFN-stimulated gene 15 (ISG15) deubiquitinase (DUB) USP18 as having antineoplastic activity by regulating lung cancer growth and oncoprotein stability. This study demonstrates that USP18 affects the stability of the KRAS oncoprotein. Interestingly, loss of USP18 reduced KRAS expression, and engineered gain of USP18 expression increased KRAS protein levels in lung cancer cells. Using the protein synthesis inhibitor cycloheximide, USP18 knockdown significantly reduced the half-life of KRAS, but gain of USP18 expression significantly increased its stability. Intriguingly, loss of USP18 altered KRAS subcellular localization by mislocalizing KRAS from the plasma membrane. To explore the biologic consequences, immunohistochemical (IHC) expression profiles of USP18 were compared in lung cancers of
versus cyclin E engineered mouse models. USP18 expression was higher in
-driven murine lung cancers, indicating a link between KRAS and USP18 expression
To solidify this association, loss of
in
/
mice was found to significantly reduce lung cancers as compared with parental
mice. Finally, translational relevance was confirmed in a human lung cancer panel by showing that USP18 IHC expression was significantly higher in
-mutant versus wild-type lung adenocarcinomas.
Taken together, this study highlights a new way to combat the oncogenic consequences of activated KRAS in lung cancer by inhibiting the DUB USP18.
. |
| doi_str_mv | 10.1158/1541-7786.MCR-16-0369 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5635999</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1984325151</sourcerecordid><originalsourceid>FETCH-LOGICAL-c505t-5e87794f39e10a9dab7d050451e34bae6fc5bbbc583c35d2939a51a2d53bfc873</originalsourceid><addsrcrecordid>eNpVUdtOwzAMjRAIxuUTQJV4LsRN3SYvSNPGTXQCbew5StIUgrp2a1Yk-HpabUzwZMs-PrbPIeQc6BUA8mvAGMI05cnVZDQNIQkpS8QeGQBiGjKIcL_Pt5gjcuz9B6URhTQ5JEcRj-KIAwzI09i22q1at3aV8jaYz16AB1ntfTBxvqyNKt239YGq8mBs_Vpptyk8TYezwFVB1lZvwUhVxjan5KBQpbdn23hC5ne3r6OHMHu-fxwNs9AgxXWIlqepiAsmLFAlcqXTnCKNESyLtbJJYVBrbZAzwzCPBBMKQUU5Ml0YnrITcrPhXbZ6YXNjq3WjSrls3EI1X7JWTv7vVO5dvtWfEhOGQoiO4HJL0NSrtvtKftRtU3U3SxA8ZhECQofCDco0nRyNLXYbgMreA9nrK3t9ZeeBhET2HnRzF3_P2039is5-AHNdgrA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1984325151</pqid></control><display><type>article</type><title>Deubiquitinase USP18 Loss Mislocalizes and Destabilizes KRAS in Lung Cancer</title><source>MEDLINE</source><source>American Association for Cancer Research</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Free Full-Text Journals in Chemistry</source><creator>Mustachio, Lisa Maria ; Lu, Yun ; Tafe, Laura J ; Memoli, Vincent ; Rodriguez-Canales, Jaime ; Mino, Barbara ; Villalobos, Pamela Andrea ; Wistuba, Ignacio ; Katayama, Hiroyuki ; Hanash, Samir M ; Roszik, Jason ; Kawakami, Masanori ; Cho, Kwang-Jin ; Hancock, John F ; Chinyengetere, Fadzai ; Hu, Shanhu ; Liu, Xi ; Freemantle, Sarah J ; Dmitrovsky, Ethan</creator><creatorcontrib>Mustachio, Lisa Maria ; Lu, Yun ; Tafe, Laura J ; Memoli, Vincent ; Rodriguez-Canales, Jaime ; Mino, Barbara ; Villalobos, Pamela Andrea ; Wistuba, Ignacio ; Katayama, Hiroyuki ; Hanash, Samir M ; Roszik, Jason ; Kawakami, Masanori ; Cho, Kwang-Jin ; Hancock, John F ; Chinyengetere, Fadzai ; Hu, Shanhu ; Liu, Xi ; Freemantle, Sarah J ; Dmitrovsky, Ethan</creatorcontrib><description>is frequently mutated in lung cancers and is associated with aggressive biology and chemotherapy resistance. Therefore, innovative approaches are needed to treat these lung cancers. Prior work implicated the IFN-stimulated gene 15 (ISG15) deubiquitinase (DUB) USP18 as having antineoplastic activity by regulating lung cancer growth and oncoprotein stability. This study demonstrates that USP18 affects the stability of the KRAS oncoprotein. Interestingly, loss of USP18 reduced KRAS expression, and engineered gain of USP18 expression increased KRAS protein levels in lung cancer cells. Using the protein synthesis inhibitor cycloheximide, USP18 knockdown significantly reduced the half-life of KRAS, but gain of USP18 expression significantly increased its stability. Intriguingly, loss of USP18 altered KRAS subcellular localization by mislocalizing KRAS from the plasma membrane. To explore the biologic consequences, immunohistochemical (IHC) expression profiles of USP18 were compared in lung cancers of
versus cyclin E engineered mouse models. USP18 expression was higher in
-driven murine lung cancers, indicating a link between KRAS and USP18 expression
To solidify this association, loss of
in
/
mice was found to significantly reduce lung cancers as compared with parental
mice. Finally, translational relevance was confirmed in a human lung cancer panel by showing that USP18 IHC expression was significantly higher in
-mutant versus wild-type lung adenocarcinomas.
Taken together, this study highlights a new way to combat the oncogenic consequences of activated KRAS in lung cancer by inhibiting the DUB USP18.
.</description><identifier>ISSN: 1541-7786</identifier><identifier>EISSN: 1557-3125</identifier><identifier>DOI: 10.1158/1541-7786.MCR-16-0369</identifier><identifier>PMID: 28242811</identifier><language>eng</language><publisher>United States: American Association for Cancer Research Inc</publisher><subject>Adenocarcinoma - drug therapy ; Adenocarcinoma - genetics ; Adenocarcinoma - pathology ; Adenocarcinoma of Lung ; Animal models ; Animals ; Cancer ; Carcinogenesis - genetics ; Cell Line, Tumor ; Cell Membrane - genetics ; Chemoresistance ; Chemotherapy ; Cyclin E ; Cyclin E - genetics ; Cycloheximide ; Cycloheximide - administration & dosage ; Disease Models, Animal ; Endopeptidases - genetics ; Female ; Gene Expression Regulation, Neoplastic - drug effects ; Gene Knockdown Techniques ; Health risk assessment ; Humans ; Interferon ; K-Ras protein ; Localization ; Lung cancer ; Lung Neoplasms - drug therapy ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Male ; Mice ; Mice, Knockout ; Mutation ; Protein biosynthesis ; Protein Biosynthesis - drug effects ; Protein synthesis ; Proto-Oncogene Proteins p21(ras) - genetics ; Stability ; USP18 protein</subject><ispartof>Molecular cancer research, 2017-07, Vol.15 (7), p.905-914</ispartof><rights>2017 American Association for Cancer Research.</rights><rights>Copyright American Association for Cancer Research Inc Jul 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c505t-5e87794f39e10a9dab7d050451e34bae6fc5bbbc583c35d2939a51a2d53bfc873</citedby><cites>FETCH-LOGICAL-c505t-5e87794f39e10a9dab7d050451e34bae6fc5bbbc583c35d2939a51a2d53bfc873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3343,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28242811$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mustachio, Lisa Maria</creatorcontrib><creatorcontrib>Lu, Yun</creatorcontrib><creatorcontrib>Tafe, Laura J</creatorcontrib><creatorcontrib>Memoli, Vincent</creatorcontrib><creatorcontrib>Rodriguez-Canales, Jaime</creatorcontrib><creatorcontrib>Mino, Barbara</creatorcontrib><creatorcontrib>Villalobos, Pamela Andrea</creatorcontrib><creatorcontrib>Wistuba, Ignacio</creatorcontrib><creatorcontrib>Katayama, Hiroyuki</creatorcontrib><creatorcontrib>Hanash, Samir M</creatorcontrib><creatorcontrib>Roszik, Jason</creatorcontrib><creatorcontrib>Kawakami, Masanori</creatorcontrib><creatorcontrib>Cho, Kwang-Jin</creatorcontrib><creatorcontrib>Hancock, John F</creatorcontrib><creatorcontrib>Chinyengetere, Fadzai</creatorcontrib><creatorcontrib>Hu, Shanhu</creatorcontrib><creatorcontrib>Liu, Xi</creatorcontrib><creatorcontrib>Freemantle, Sarah J</creatorcontrib><creatorcontrib>Dmitrovsky, Ethan</creatorcontrib><title>Deubiquitinase USP18 Loss Mislocalizes and Destabilizes KRAS in Lung Cancer</title><title>Molecular cancer research</title><addtitle>Mol Cancer Res</addtitle><description>is frequently mutated in lung cancers and is associated with aggressive biology and chemotherapy resistance. Therefore, innovative approaches are needed to treat these lung cancers. Prior work implicated the IFN-stimulated gene 15 (ISG15) deubiquitinase (DUB) USP18 as having antineoplastic activity by regulating lung cancer growth and oncoprotein stability. This study demonstrates that USP18 affects the stability of the KRAS oncoprotein. Interestingly, loss of USP18 reduced KRAS expression, and engineered gain of USP18 expression increased KRAS protein levels in lung cancer cells. Using the protein synthesis inhibitor cycloheximide, USP18 knockdown significantly reduced the half-life of KRAS, but gain of USP18 expression significantly increased its stability. Intriguingly, loss of USP18 altered KRAS subcellular localization by mislocalizing KRAS from the plasma membrane. To explore the biologic consequences, immunohistochemical (IHC) expression profiles of USP18 were compared in lung cancers of
versus cyclin E engineered mouse models. USP18 expression was higher in
-driven murine lung cancers, indicating a link between KRAS and USP18 expression
To solidify this association, loss of
in
/
mice was found to significantly reduce lung cancers as compared with parental
mice. Finally, translational relevance was confirmed in a human lung cancer panel by showing that USP18 IHC expression was significantly higher in
-mutant versus wild-type lung adenocarcinomas.
Taken together, this study highlights a new way to combat the oncogenic consequences of activated KRAS in lung cancer by inhibiting the DUB USP18.
.</description><subject>Adenocarcinoma - drug therapy</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - pathology</subject><subject>Adenocarcinoma of Lung</subject><subject>Animal models</subject><subject>Animals</subject><subject>Cancer</subject><subject>Carcinogenesis - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Membrane - genetics</subject><subject>Chemoresistance</subject><subject>Chemotherapy</subject><subject>Cyclin E</subject><subject>Cyclin E - genetics</subject><subject>Cycloheximide</subject><subject>Cycloheximide - administration & dosage</subject><subject>Disease Models, Animal</subject><subject>Endopeptidases - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Gene Knockdown Techniques</subject><subject>Health risk assessment</subject><subject>Humans</subject><subject>Interferon</subject><subject>K-Ras protein</subject><subject>Localization</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mutation</subject><subject>Protein biosynthesis</subject><subject>Protein Biosynthesis - drug effects</subject><subject>Protein synthesis</subject><subject>Proto-Oncogene Proteins p21(ras) - genetics</subject><subject>Stability</subject><subject>USP18 protein</subject><issn>1541-7786</issn><issn>1557-3125</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUdtOwzAMjRAIxuUTQJV4LsRN3SYvSNPGTXQCbew5StIUgrp2a1Yk-HpabUzwZMs-PrbPIeQc6BUA8mvAGMI05cnVZDQNIQkpS8QeGQBiGjKIcL_Pt5gjcuz9B6URhTQ5JEcRj-KIAwzI09i22q1at3aV8jaYz16AB1ntfTBxvqyNKt239YGq8mBs_Vpptyk8TYezwFVB1lZvwUhVxjan5KBQpbdn23hC5ne3r6OHMHu-fxwNs9AgxXWIlqepiAsmLFAlcqXTnCKNESyLtbJJYVBrbZAzwzCPBBMKQUU5Ml0YnrITcrPhXbZ6YXNjq3WjSrls3EI1X7JWTv7vVO5dvtWfEhOGQoiO4HJL0NSrtvtKftRtU3U3SxA8ZhECQofCDco0nRyNLXYbgMreA9nrK3t9ZeeBhET2HnRzF3_P2039is5-AHNdgrA</recordid><startdate>20170701</startdate><enddate>20170701</enddate><creator>Mustachio, Lisa Maria</creator><creator>Lu, Yun</creator><creator>Tafe, Laura J</creator><creator>Memoli, Vincent</creator><creator>Rodriguez-Canales, Jaime</creator><creator>Mino, Barbara</creator><creator>Villalobos, Pamela Andrea</creator><creator>Wistuba, Ignacio</creator><creator>Katayama, Hiroyuki</creator><creator>Hanash, Samir M</creator><creator>Roszik, Jason</creator><creator>Kawakami, Masanori</creator><creator>Cho, Kwang-Jin</creator><creator>Hancock, John F</creator><creator>Chinyengetere, Fadzai</creator><creator>Hu, Shanhu</creator><creator>Liu, Xi</creator><creator>Freemantle, Sarah J</creator><creator>Dmitrovsky, Ethan</creator><general>American Association for Cancer Research Inc</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>7TO</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20170701</creationdate><title>Deubiquitinase USP18 Loss Mislocalizes and Destabilizes KRAS in Lung Cancer</title><author>Mustachio, Lisa Maria ; Lu, Yun ; Tafe, Laura J ; Memoli, Vincent ; Rodriguez-Canales, Jaime ; Mino, Barbara ; Villalobos, Pamela Andrea ; Wistuba, Ignacio ; Katayama, Hiroyuki ; Hanash, Samir M ; Roszik, Jason ; Kawakami, Masanori ; Cho, Kwang-Jin ; Hancock, John F ; Chinyengetere, Fadzai ; Hu, Shanhu ; Liu, Xi ; Freemantle, Sarah J ; Dmitrovsky, Ethan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c505t-5e87794f39e10a9dab7d050451e34bae6fc5bbbc583c35d2939a51a2d53bfc873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adenocarcinoma - drug therapy</topic><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - pathology</topic><topic>Adenocarcinoma of Lung</topic><topic>Animal models</topic><topic>Animals</topic><topic>Cancer</topic><topic>Carcinogenesis - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cell Membrane - genetics</topic><topic>Chemoresistance</topic><topic>Chemotherapy</topic><topic>Cyclin E</topic><topic>Cyclin E - genetics</topic><topic>Cycloheximide</topic><topic>Cycloheximide - administration & dosage</topic><topic>Disease Models, Animal</topic><topic>Endopeptidases - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Gene Knockdown Techniques</topic><topic>Health risk assessment</topic><topic>Humans</topic><topic>Interferon</topic><topic>K-Ras protein</topic><topic>Localization</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mutation</topic><topic>Protein biosynthesis</topic><topic>Protein Biosynthesis - drug effects</topic><topic>Protein synthesis</topic><topic>Proto-Oncogene Proteins p21(ras) - genetics</topic><topic>Stability</topic><topic>USP18 protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mustachio, Lisa Maria</creatorcontrib><creatorcontrib>Lu, Yun</creatorcontrib><creatorcontrib>Tafe, Laura J</creatorcontrib><creatorcontrib>Memoli, Vincent</creatorcontrib><creatorcontrib>Rodriguez-Canales, Jaime</creatorcontrib><creatorcontrib>Mino, Barbara</creatorcontrib><creatorcontrib>Villalobos, Pamela Andrea</creatorcontrib><creatorcontrib>Wistuba, Ignacio</creatorcontrib><creatorcontrib>Katayama, Hiroyuki</creatorcontrib><creatorcontrib>Hanash, Samir M</creatorcontrib><creatorcontrib>Roszik, Jason</creatorcontrib><creatorcontrib>Kawakami, Masanori</creatorcontrib><creatorcontrib>Cho, Kwang-Jin</creatorcontrib><creatorcontrib>Hancock, John F</creatorcontrib><creatorcontrib>Chinyengetere, Fadzai</creatorcontrib><creatorcontrib>Hu, Shanhu</creatorcontrib><creatorcontrib>Liu, Xi</creatorcontrib><creatorcontrib>Freemantle, Sarah J</creatorcontrib><creatorcontrib>Dmitrovsky, Ethan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mustachio, Lisa Maria</au><au>Lu, Yun</au><au>Tafe, Laura J</au><au>Memoli, Vincent</au><au>Rodriguez-Canales, Jaime</au><au>Mino, Barbara</au><au>Villalobos, Pamela Andrea</au><au>Wistuba, Ignacio</au><au>Katayama, Hiroyuki</au><au>Hanash, Samir M</au><au>Roszik, Jason</au><au>Kawakami, Masanori</au><au>Cho, Kwang-Jin</au><au>Hancock, John F</au><au>Chinyengetere, Fadzai</au><au>Hu, Shanhu</au><au>Liu, Xi</au><au>Freemantle, Sarah J</au><au>Dmitrovsky, Ethan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deubiquitinase USP18 Loss Mislocalizes and Destabilizes KRAS in Lung Cancer</atitle><jtitle>Molecular cancer research</jtitle><addtitle>Mol Cancer Res</addtitle><date>2017-07-01</date><risdate>2017</risdate><volume>15</volume><issue>7</issue><spage>905</spage><epage>914</epage><pages>905-914</pages><issn>1541-7786</issn><eissn>1557-3125</eissn><abstract>is frequently mutated in lung cancers and is associated with aggressive biology and chemotherapy resistance. Therefore, innovative approaches are needed to treat these lung cancers. Prior work implicated the IFN-stimulated gene 15 (ISG15) deubiquitinase (DUB) USP18 as having antineoplastic activity by regulating lung cancer growth and oncoprotein stability. This study demonstrates that USP18 affects the stability of the KRAS oncoprotein. Interestingly, loss of USP18 reduced KRAS expression, and engineered gain of USP18 expression increased KRAS protein levels in lung cancer cells. Using the protein synthesis inhibitor cycloheximide, USP18 knockdown significantly reduced the half-life of KRAS, but gain of USP18 expression significantly increased its stability. Intriguingly, loss of USP18 altered KRAS subcellular localization by mislocalizing KRAS from the plasma membrane. To explore the biologic consequences, immunohistochemical (IHC) expression profiles of USP18 were compared in lung cancers of
versus cyclin E engineered mouse models. USP18 expression was higher in
-driven murine lung cancers, indicating a link between KRAS and USP18 expression
To solidify this association, loss of
in
/
mice was found to significantly reduce lung cancers as compared with parental
mice. Finally, translational relevance was confirmed in a human lung cancer panel by showing that USP18 IHC expression was significantly higher in
-mutant versus wild-type lung adenocarcinomas.
Taken together, this study highlights a new way to combat the oncogenic consequences of activated KRAS in lung cancer by inhibiting the DUB USP18.
.</abstract><cop>United States</cop><pub>American Association for Cancer Research Inc</pub><pmid>28242811</pmid><doi>10.1158/1541-7786.MCR-16-0369</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Association for Cancer Research; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Free Full-Text Journals in Chemistry |
| subjects | Adenocarcinoma - drug therapy Adenocarcinoma - genetics Adenocarcinoma - pathology Adenocarcinoma of Lung Animal models Animals Cancer Carcinogenesis - genetics Cell Line, Tumor Cell Membrane - genetics Chemoresistance Chemotherapy Cyclin E Cyclin E - genetics Cycloheximide Cycloheximide - administration & dosage Disease Models, Animal Endopeptidases - genetics Female Gene Expression Regulation, Neoplastic - drug effects Gene Knockdown Techniques Health risk assessment Humans Interferon K-Ras protein Localization Lung cancer Lung Neoplasms - drug therapy Lung Neoplasms - genetics Lung Neoplasms - pathology Male Mice Mice, Knockout Mutation Protein biosynthesis Protein Biosynthesis - drug effects Protein synthesis Proto-Oncogene Proteins p21(ras) - genetics Stability USP18 protein |
| title | Deubiquitinase USP18 Loss Mislocalizes and Destabilizes KRAS in Lung Cancer |
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