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The Tumor Suppressor SOCS1 Diminishes Tolerance to Oxidative Stress in Hepatocellular Carcinoma
SOCS1 is a tumor suppressor in hepatocellular carcinoma (HCC). Recently, we showed that a loss of SOCS1 in hepatocytes promotes NRF2 activation. Here, we investigated how SOCS1 expression in HCC cells affected oxidative stress response and modulated the cellular proteome. Murine Hepa1-6 cells expres...
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Published in: | Cancers 2024-01, Vol.16 (2), p.292 |
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creator | Shukla, Akhil Khan, Md Gulam Musawwir Cayarga, Anny Armas Namvarpour, Mozhdeh Chowdhury, Mohammad Mobarak H Levesque, Dominique Lucier, Jean-François Boisvert, François-Michel Ramanathan, Sheela Ilangumaran, Subburaj |
description | SOCS1 is a tumor suppressor in hepatocellular carcinoma (HCC). Recently, we showed that a loss of SOCS1 in hepatocytes promotes NRF2 activation. Here, we investigated how SOCS1 expression in HCC cells affected oxidative stress response and modulated the cellular proteome. Murine Hepa1-6 cells expressing SOCS1 (Hepa-SOCS1) or control vector (Hepa-Vector) were treated with cisplatin or tert-butyl hydroperoxide (
-BHP). The induction of NRF2 and its target genes, oxidative stress, lipid peroxidation, cell survival and cellular proteome profiles were evaluated. NRF2 induction was significantly reduced in Hepa-SOCS1 cells. The gene and protein expression of NRF2 targets were differentially induced in Hepa-Vector cells but markedly suppressed in Hepa-SOCS1 cells. Hepa-SOCS1 cells displayed an increased induction of reactive oxygen species but reduced lipid peroxidation. Nonetheless, Hepa-SOCS1 cells treated with cisplatin or
-BHP showed reduced survival.
, poorly induced in Hepa-SOCS1 cells, showed a strong positive correlation with
and an inverse correlation with
in the TCGA-LIHC transcriptomic data. A proteomic analysis of Hepa-Vector and Hepa-SOCS1 cells revealed that SOCS1 differentially modulated many proteins involved in diverse molecular pathways, including mitochondrial ROS generation and ROS detoxification, through peroxiredoxin and thioredoxin systems. Our findings indicate that maintaining sensitivity to oxidative stress is an important tumor suppression mechanism of SOCS1 in HCC. |
doi_str_mv | 10.3390/cancers16020292 |
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-BHP). The induction of NRF2 and its target genes, oxidative stress, lipid peroxidation, cell survival and cellular proteome profiles were evaluated. NRF2 induction was significantly reduced in Hepa-SOCS1 cells. The gene and protein expression of NRF2 targets were differentially induced in Hepa-Vector cells but markedly suppressed in Hepa-SOCS1 cells. Hepa-SOCS1 cells displayed an increased induction of reactive oxygen species but reduced lipid peroxidation. Nonetheless, Hepa-SOCS1 cells treated with cisplatin or
-BHP showed reduced survival.
, poorly induced in Hepa-SOCS1 cells, showed a strong positive correlation with
and an inverse correlation with
in the TCGA-LIHC transcriptomic data. A proteomic analysis of Hepa-Vector and Hepa-SOCS1 cells revealed that SOCS1 differentially modulated many proteins involved in diverse molecular pathways, including mitochondrial ROS generation and ROS detoxification, through peroxiredoxin and thioredoxin systems. Our findings indicate that maintaining sensitivity to oxidative stress is an important tumor suppression mechanism of SOCS1 in HCC.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers16020292</identifier><identifier>PMID: 38254783</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Antibodies ; Butyl hydroperoxide ; Cell survival ; Cells ; Cellular stress response ; Cisplatin ; Cyclin-dependent kinases ; Cytokines ; Detoxification ; Development and progression ; Gene expression ; Genes ; Growth factors ; Hepatocellular carcinoma ; Hepatocytes ; Hepatoma ; Kinases ; Leukemia ; Lipid peroxidation ; Lipids ; Liver cancer ; Oxidative stress ; Peroxiredoxin ; Proteins ; Proteomes ; Proteomics ; Reactive oxygen species ; Thioredoxin ; Transcriptomics ; Tumor suppression ; Tumor suppressor genes ; Tumors</subject><ispartof>Cancers, 2024-01, Vol.16 (2), p.292</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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-c433t-230420301717fc9992ef8cb7a7086730eac678660735324dbd32c33293f556253</citedby><cites>FETCH-LOGICAL-c433t-230420301717fc9992ef8cb7a7086730eac678660735324dbd32c33293f556253</cites><orcidid>0000-0002-7563-576X ; 0000-0001-7424-580X ; 0000-0002-0787-4523</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2918570718/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2918570718?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,25753,27924,27925,37012,37013,44590,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38254783$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shukla, Akhil</creatorcontrib><creatorcontrib>Khan, Md Gulam Musawwir</creatorcontrib><creatorcontrib>Cayarga, Anny Armas</creatorcontrib><creatorcontrib>Namvarpour, Mozhdeh</creatorcontrib><creatorcontrib>Chowdhury, Mohammad Mobarak H</creatorcontrib><creatorcontrib>Levesque, Dominique</creatorcontrib><creatorcontrib>Lucier, Jean-François</creatorcontrib><creatorcontrib>Boisvert, François-Michel</creatorcontrib><creatorcontrib>Ramanathan, Sheela</creatorcontrib><creatorcontrib>Ilangumaran, Subburaj</creatorcontrib><title>The Tumor Suppressor SOCS1 Diminishes Tolerance to Oxidative Stress in Hepatocellular Carcinoma</title><title>Cancers</title><addtitle>Cancers (Basel)</addtitle><description>SOCS1 is a tumor suppressor in hepatocellular carcinoma (HCC). Recently, we showed that a loss of SOCS1 in hepatocytes promotes NRF2 activation. Here, we investigated how SOCS1 expression in HCC cells affected oxidative stress response and modulated the cellular proteome. Murine Hepa1-6 cells expressing SOCS1 (Hepa-SOCS1) or control vector (Hepa-Vector) were treated with cisplatin or tert-butyl hydroperoxide (
-BHP). The induction of NRF2 and its target genes, oxidative stress, lipid peroxidation, cell survival and cellular proteome profiles were evaluated. NRF2 induction was significantly reduced in Hepa-SOCS1 cells. The gene and protein expression of NRF2 targets were differentially induced in Hepa-Vector cells but markedly suppressed in Hepa-SOCS1 cells. Hepa-SOCS1 cells displayed an increased induction of reactive oxygen species but reduced lipid peroxidation. Nonetheless, Hepa-SOCS1 cells treated with cisplatin or
-BHP showed reduced survival.
, poorly induced in Hepa-SOCS1 cells, showed a strong positive correlation with
and an inverse correlation with
in the TCGA-LIHC transcriptomic data. A proteomic analysis of Hepa-Vector and Hepa-SOCS1 cells revealed that SOCS1 differentially modulated many proteins involved in diverse molecular pathways, including mitochondrial ROS generation and ROS detoxification, through peroxiredoxin and thioredoxin systems. Our findings indicate that maintaining sensitivity to oxidative stress is an important tumor suppression mechanism of SOCS1 in HCC.</description><subject>Antibodies</subject><subject>Butyl hydroperoxide</subject><subject>Cell survival</subject><subject>Cells</subject><subject>Cellular stress response</subject><subject>Cisplatin</subject><subject>Cyclin-dependent kinases</subject><subject>Cytokines</subject><subject>Detoxification</subject><subject>Development and progression</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Growth factors</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatocytes</subject><subject>Hepatoma</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Liver cancer</subject><subject>Oxidative stress</subject><subject>Peroxiredoxin</subject><subject>Proteins</subject><subject>Proteomes</subject><subject>Proteomics</subject><subject>Reactive oxygen species</subject><subject>Thioredoxin</subject><subject>Transcriptomics</subject><subject>Tumor suppression</subject><subject>Tumor suppressor genes</subject><subject>Tumors</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNptkc1r3DAQxUVpacI2596CoJdeNpFmbEk-hk3aFAJ72O1ZaOVxomBbrmSH5L-vTdKvUM1Bw_B7Mw8eYx-lOEOsxLl3vaeUpRIgoII37BiEhrVSVfH2r_6IneR8L-aHKLXS79kRGigLbfCY2f0d8f3UxcR30zAkynlpt5ud5JehC33Id5T5PraUlnN8jHz7GGo3hgfiu3ER8NDzaxrcGD217dS6xDcu-dDHzn1g7xrXZjp5-Vfs-5er_eZ6fbP9-m1zcbP2BeK4BhQFCBRSS934qqqAGuMP2mlhlEZBzittlBIaS4SiPtQIHhEqbMpSQYkr9vl575Dij4nyaLuQFzuupzhlC5Vc9AZgRj-9Qu_jlPrZ3UKZUgstzR_q1rVkQ9_EMTm_LLUX2gijwRg1U2f_oeaqqQs-9tSEef6P4PxZ4FPMOVFjhxQ6l56sFHZJ1b5KdVacvtidDh3Vv_lfGeJPTEGasA</recordid><startdate>20240101</startdate><enddate>20240101</enddate><creator>Shukla, Akhil</creator><creator>Khan, Md Gulam Musawwir</creator><creator>Cayarga, Anny Armas</creator><creator>Namvarpour, Mozhdeh</creator><creator>Chowdhury, Mohammad Mobarak H</creator><creator>Levesque, Dominique</creator><creator>Lucier, Jean-François</creator><creator>Boisvert, François-Michel</creator><creator>Ramanathan, Sheela</creator><creator>Ilangumaran, Subburaj</creator><general>MDPI AG</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>8G5</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>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7563-576X</orcidid><orcidid>https://orcid.org/0000-0001-7424-580X</orcidid><orcidid>https://orcid.org/0000-0002-0787-4523</orcidid></search><sort><creationdate>20240101</creationdate><title>The Tumor Suppressor SOCS1 Diminishes Tolerance to Oxidative Stress in Hepatocellular Carcinoma</title><author>Shukla, Akhil ; Khan, Md Gulam Musawwir ; Cayarga, Anny Armas ; Namvarpour, Mozhdeh ; Chowdhury, Mohammad Mobarak H ; Levesque, Dominique ; Lucier, Jean-François ; Boisvert, François-Michel ; Ramanathan, Sheela ; Ilangumaran, Subburaj</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c433t-230420301717fc9992ef8cb7a7086730eac678660735324dbd32c33293f556253</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Antibodies</topic><topic>Butyl hydroperoxide</topic><topic>Cell survival</topic><topic>Cells</topic><topic>Cellular stress response</topic><topic>Cisplatin</topic><topic>Cyclin-dependent kinases</topic><topic>Cytokines</topic><topic>Detoxification</topic><topic>Development and progression</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Growth factors</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatocytes</topic><topic>Hepatoma</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Lipid peroxidation</topic><topic>Lipids</topic><topic>Liver cancer</topic><topic>Oxidative stress</topic><topic>Peroxiredoxin</topic><topic>Proteins</topic><topic>Proteomes</topic><topic>Proteomics</topic><topic>Reactive oxygen species</topic><topic>Thioredoxin</topic><topic>Transcriptomics</topic><topic>Tumor suppression</topic><topic>Tumor suppressor genes</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shukla, Akhil</creatorcontrib><creatorcontrib>Khan, Md Gulam Musawwir</creatorcontrib><creatorcontrib>Cayarga, Anny Armas</creatorcontrib><creatorcontrib>Namvarpour, Mozhdeh</creatorcontrib><creatorcontrib>Chowdhury, Mohammad Mobarak H</creatorcontrib><creatorcontrib>Levesque, Dominique</creatorcontrib><creatorcontrib>Lucier, Jean-François</creatorcontrib><creatorcontrib>Boisvert, François-Michel</creatorcontrib><creatorcontrib>Ramanathan, Sheela</creatorcontrib><creatorcontrib>Ilangumaran, Subburaj</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>ProQuest research library</collection><collection>ProQuest Biological Science Journals</collection><collection>Research Library (Corporate)</collection><collection>ProQuest - 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 Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shukla, Akhil</au><au>Khan, Md Gulam Musawwir</au><au>Cayarga, Anny Armas</au><au>Namvarpour, Mozhdeh</au><au>Chowdhury, Mohammad Mobarak H</au><au>Levesque, Dominique</au><au>Lucier, Jean-François</au><au>Boisvert, François-Michel</au><au>Ramanathan, Sheela</au><au>Ilangumaran, Subburaj</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Tumor Suppressor SOCS1 Diminishes Tolerance to Oxidative Stress in Hepatocellular Carcinoma</atitle><jtitle>Cancers</jtitle><addtitle>Cancers (Basel)</addtitle><date>2024-01-01</date><risdate>2024</risdate><volume>16</volume><issue>2</issue><spage>292</spage><pages>292-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>SOCS1 is a tumor suppressor in hepatocellular carcinoma (HCC). Recently, we showed that a loss of SOCS1 in hepatocytes promotes NRF2 activation. Here, we investigated how SOCS1 expression in HCC cells affected oxidative stress response and modulated the cellular proteome. Murine Hepa1-6 cells expressing SOCS1 (Hepa-SOCS1) or control vector (Hepa-Vector) were treated with cisplatin or tert-butyl hydroperoxide (
-BHP). The induction of NRF2 and its target genes, oxidative stress, lipid peroxidation, cell survival and cellular proteome profiles were evaluated. NRF2 induction was significantly reduced in Hepa-SOCS1 cells. The gene and protein expression of NRF2 targets were differentially induced in Hepa-Vector cells but markedly suppressed in Hepa-SOCS1 cells. Hepa-SOCS1 cells displayed an increased induction of reactive oxygen species but reduced lipid peroxidation. Nonetheless, Hepa-SOCS1 cells treated with cisplatin or
-BHP showed reduced survival.
, poorly induced in Hepa-SOCS1 cells, showed a strong positive correlation with
and an inverse correlation with
in the TCGA-LIHC transcriptomic data. A proteomic analysis of Hepa-Vector and Hepa-SOCS1 cells revealed that SOCS1 differentially modulated many proteins involved in diverse molecular pathways, including mitochondrial ROS generation and ROS detoxification, through peroxiredoxin and thioredoxin systems. Our findings indicate that maintaining sensitivity to oxidative stress is an important tumor suppression mechanism of SOCS1 in HCC.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>38254783</pmid><doi>10.3390/cancers16020292</doi><orcidid>https://orcid.org/0000-0002-7563-576X</orcidid><orcidid>https://orcid.org/0000-0001-7424-580X</orcidid><orcidid>https://orcid.org/0000-0002-0787-4523</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Antibodies Butyl hydroperoxide Cell survival Cells Cellular stress response Cisplatin Cyclin-dependent kinases Cytokines Detoxification Development and progression Gene expression Genes Growth factors Hepatocellular carcinoma Hepatocytes Hepatoma Kinases Leukemia Lipid peroxidation Lipids Liver cancer Oxidative stress Peroxiredoxin Proteins Proteomes Proteomics Reactive oxygen species Thioredoxin Transcriptomics Tumor suppression Tumor suppressor genes Tumors |
title | The Tumor Suppressor SOCS1 Diminishes Tolerance to Oxidative Stress in Hepatocellular Carcinoma |
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