Oncofetal HLF transactivates c-Jun to promote hepatocellular carcinoma development and sorafenib resistance
Background and aimsThe unique expression pattern makes oncofetal proteins ideal diagnostic biomarkers and therapeutic targets in cancer. However, few oncofetal proteins have been identified and entered clinical practice.MethodsFetal liver, adult liver and hepatocellular carcinoma (HCC) tissues were...
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| Veröffentlicht in: | Gut 2019-10, Vol.68 (10), p.1858-1871 |
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| creator | Xiang, Dai-Min Sun, Wen Zhou, Tengfei Zhang, Cheng Cheng, Zhuo Li, Shi-Chao Jiang, Weiqi Wang, Ruoyu Fu, Gongbo Cui, Xiuliang Hou, Guojun Jin, Guang-Zhi Li, Hengyu Hou, Caiying Liu, Hui Wang, Hongyang Ding, Jin |
| description | Background and aimsThe unique expression pattern makes oncofetal proteins ideal diagnostic biomarkers and therapeutic targets in cancer. However, few oncofetal proteins have been identified and entered clinical practice.MethodsFetal liver, adult liver and hepatocellular carcinoma (HCC) tissues were employed to assess the expression of hepatic leukaemia factor (HLF). The impact of HLF on HCC onset and progression was investigated both in vivo and in vitro. The association between HLF and patient prognosis was determined in patient cohorts. The correlation between HLF expression and sorafenib benefits in HCC was further evaluated in patient cohorts and patient-derived xenografts (PDXs).ResultsHLF is a novel oncofetal protein which is reactivated in HCC by SOX2 and OCT4. Functional studies revealed that HLF transactivates c-Jun to promote tumour initiating cell (TIC) generation and enhances TIC-like properties of hepatoma cells, thus driving HCC initiation and progression. Consistently, our clinical investigations elucidated the association between HLF and patient prognosis and unravelled the close correlation between HLF levels and c-Jun expression in patient HCCs. Importantly, HLF/c-Jun axis determines the responses of hepatoma cells to sorafenib treatment, and interference of HLF abrogated c-Jun activation and enhanced sorafenib response. Analysis of patient cohorts and PDXs further suggests that HLF/c-Jun axis might serve as a biomarker for sorafenib benefits in HCC patients.ConclusionsOur findings uncovered HLF as a novel oncofetal protein and revealed the crucial role of the HLF/c-Jun axis in HCC development and sorafenib response, rendering HLF as an optimal target for the prevention and intervention of HCC. |
| doi_str_mv | 10.1136/gutjnl-2018-317440 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2288795662</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2288795662</sourcerecordid><originalsourceid>FETCH-LOGICAL-b474t-fe9e3870781e5f9983c4845fb8350b42a33c4315cec098fb603eda64fc4ab4c43</originalsourceid><addsrcrecordid>eNqNkEFPwyAYhonRuDn9Ax4MiedOKLSlR7M4p1myi54byj60s4UJdIn_XpbOeTOeCPC87_flQeiakimlLL9768PGtElKqEgYLTgnJ2hMeR5vqRCnaEwILZKs4OUIXXi_IYQIUdJzNGKUUpHyYow-VkZZDUG2eLGc4-Ck8VKFZicDeKyS597gYPHW2c4GwO-wlcEqaNu-lQ4r6VRjbCfxGnbQ2m0HJmBp1thbJzWYpsYOfOODNAou0ZmWrYerwzlBr_OHl9kiWa4en2b3y6TmBQ-JhhKYKEghKGS6LAVTXPBM14JlpOapZPGB0UyBIqXQdU4YrGXOteKy5vFrgm6H3rj1Zw8-VBvbOxNHVmkUU5RZnqeRSgdKOeu9A11tXdNJ91VRUu39VoPfau-3GvzG0M2huq87WB8jP0IjkAxA3W3-Vzj95Y9r_hH4Bg_Clmw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2288795662</pqid></control><display><type>article</type><title>Oncofetal HLF transactivates c-Jun to promote hepatocellular carcinoma development and sorafenib resistance</title><source>MEDLINE</source><source>PubMed Central</source><creator>Xiang, Dai-Min ; Sun, Wen ; Zhou, Tengfei ; Zhang, Cheng ; Cheng, Zhuo ; Li, Shi-Chao ; Jiang, Weiqi ; Wang, Ruoyu ; Fu, Gongbo ; Cui, Xiuliang ; Hou, Guojun ; Jin, Guang-Zhi ; Li, Hengyu ; Hou, Caiying ; Liu, Hui ; Wang, Hongyang ; Ding, Jin</creator><creatorcontrib>Xiang, Dai-Min ; Sun, Wen ; Zhou, Tengfei ; Zhang, Cheng ; Cheng, Zhuo ; Li, Shi-Chao ; Jiang, Weiqi ; Wang, Ruoyu ; Fu, Gongbo ; Cui, Xiuliang ; Hou, Guojun ; Jin, Guang-Zhi ; Li, Hengyu ; Hou, Caiying ; Liu, Hui ; Wang, Hongyang ; Ding, Jin</creatorcontrib><description>Background and aimsThe unique expression pattern makes oncofetal proteins ideal diagnostic biomarkers and therapeutic targets in cancer. However, few oncofetal proteins have been identified and entered clinical practice.MethodsFetal liver, adult liver and hepatocellular carcinoma (HCC) tissues were employed to assess the expression of hepatic leukaemia factor (HLF). The impact of HLF on HCC onset and progression was investigated both in vivo and in vitro. The association between HLF and patient prognosis was determined in patient cohorts. The correlation between HLF expression and sorafenib benefits in HCC was further evaluated in patient cohorts and patient-derived xenografts (PDXs).ResultsHLF is a novel oncofetal protein which is reactivated in HCC by SOX2 and OCT4. Functional studies revealed that HLF transactivates c-Jun to promote tumour initiating cell (TIC) generation and enhances TIC-like properties of hepatoma cells, thus driving HCC initiation and progression. Consistently, our clinical investigations elucidated the association between HLF and patient prognosis and unravelled the close correlation between HLF levels and c-Jun expression in patient HCCs. Importantly, HLF/c-Jun axis determines the responses of hepatoma cells to sorafenib treatment, and interference of HLF abrogated c-Jun activation and enhanced sorafenib response. Analysis of patient cohorts and PDXs further suggests that HLF/c-Jun axis might serve as a biomarker for sorafenib benefits in HCC patients.ConclusionsOur findings uncovered HLF as a novel oncofetal protein and revealed the crucial role of the HLF/c-Jun axis in HCC development and sorafenib response, rendering HLF as an optimal target for the prevention and intervention of HCC.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>DOI: 10.1136/gutjnl-2018-317440</identifier><identifier>PMID: 31118247</identifier><language>eng</language><publisher>England: BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><subject>Adult ; Antineoplastic Agents - pharmacology ; Apoptosis ; Basic-Leucine Zipper Transcription Factors - biosynthesis ; Basic-Leucine Zipper Transcription Factors - genetics ; Biomarkers ; c-Jun protein ; Cancer therapies ; carcinogenesis ; Carcinoma, Hepatocellular - drug therapy ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - pathology ; Cell Line, Tumor ; Clinical medicine ; Disease Progression ; DNA, Neoplasm - genetics ; drug resistance ; Drug Resistance, Neoplasm ; Female ; Fetuses ; Gene expression ; Genes, jun - genetics ; Hepatocellular carcinoma ; Hepatology ; Hepatoma ; Hospitals ; Humans ; Immunoprecipitation ; Inhibitor drugs ; Kinases ; Leucine Zippers ; Leukemia ; Liver cancer ; Liver Neoplasms - drug therapy ; Liver Neoplasms - genetics ; Liver Neoplasms - pathology ; Male ; Medical diagnosis ; Medical prognosis ; Oct-4 protein ; oncogenes ; Patients ; Prognosis ; Proteins ; Signal transduction ; Sorafenib - pharmacology ; Stem cells ; Surgery ; Targeted cancer therapy ; Therapeutic applications ; Transcription factors ; Tumors ; tumour markers ; Xenografts</subject><ispartof>Gut, 2019-10, Vol.68 (10), p.1858-1871</ispartof><rights>Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.</rights><rights>2019 Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b474t-fe9e3870781e5f9983c4845fb8350b42a33c4315cec098fb603eda64fc4ab4c43</citedby><cites>FETCH-LOGICAL-b474t-fe9e3870781e5f9983c4845fb8350b42a33c4315cec098fb603eda64fc4ab4c43</cites><orcidid>0000-0002-4709-3334</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31118247$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xiang, Dai-Min</creatorcontrib><creatorcontrib>Sun, Wen</creatorcontrib><creatorcontrib>Zhou, Tengfei</creatorcontrib><creatorcontrib>Zhang, Cheng</creatorcontrib><creatorcontrib>Cheng, Zhuo</creatorcontrib><creatorcontrib>Li, Shi-Chao</creatorcontrib><creatorcontrib>Jiang, Weiqi</creatorcontrib><creatorcontrib>Wang, Ruoyu</creatorcontrib><creatorcontrib>Fu, Gongbo</creatorcontrib><creatorcontrib>Cui, Xiuliang</creatorcontrib><creatorcontrib>Hou, Guojun</creatorcontrib><creatorcontrib>Jin, Guang-Zhi</creatorcontrib><creatorcontrib>Li, Hengyu</creatorcontrib><creatorcontrib>Hou, Caiying</creatorcontrib><creatorcontrib>Liu, Hui</creatorcontrib><creatorcontrib>Wang, Hongyang</creatorcontrib><creatorcontrib>Ding, Jin</creatorcontrib><title>Oncofetal HLF transactivates c-Jun to promote hepatocellular carcinoma development and sorafenib resistance</title><title>Gut</title><addtitle>Gut</addtitle><addtitle>Gut</addtitle><description>Background and aimsThe unique expression pattern makes oncofetal proteins ideal diagnostic biomarkers and therapeutic targets in cancer. However, few oncofetal proteins have been identified and entered clinical practice.MethodsFetal liver, adult liver and hepatocellular carcinoma (HCC) tissues were employed to assess the expression of hepatic leukaemia factor (HLF). The impact of HLF on HCC onset and progression was investigated both in vivo and in vitro. The association between HLF and patient prognosis was determined in patient cohorts. The correlation between HLF expression and sorafenib benefits in HCC was further evaluated in patient cohorts and patient-derived xenografts (PDXs).ResultsHLF is a novel oncofetal protein which is reactivated in HCC by SOX2 and OCT4. Functional studies revealed that HLF transactivates c-Jun to promote tumour initiating cell (TIC) generation and enhances TIC-like properties of hepatoma cells, thus driving HCC initiation and progression. Consistently, our clinical investigations elucidated the association between HLF and patient prognosis and unravelled the close correlation between HLF levels and c-Jun expression in patient HCCs. Importantly, HLF/c-Jun axis determines the responses of hepatoma cells to sorafenib treatment, and interference of HLF abrogated c-Jun activation and enhanced sorafenib response. Analysis of patient cohorts and PDXs further suggests that HLF/c-Jun axis might serve as a biomarker for sorafenib benefits in HCC patients.ConclusionsOur findings uncovered HLF as a novel oncofetal protein and revealed the crucial role of the HLF/c-Jun axis in HCC development and sorafenib response, rendering HLF as an optimal target for the prevention and intervention of HCC.</description><subject>Adult</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Basic-Leucine Zipper Transcription Factors - biosynthesis</subject><subject>Basic-Leucine Zipper Transcription Factors - genetics</subject><subject>Biomarkers</subject><subject>c-Jun protein</subject><subject>Cancer therapies</subject><subject>carcinogenesis</subject><subject>Carcinoma, Hepatocellular - drug therapy</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell Line, Tumor</subject><subject>Clinical medicine</subject><subject>Disease Progression</subject><subject>DNA, Neoplasm - genetics</subject><subject>drug resistance</subject><subject>Drug Resistance, Neoplasm</subject><subject>Female</subject><subject>Fetuses</subject><subject>Gene expression</subject><subject>Genes, jun - genetics</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatology</subject><subject>Hepatoma</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Inhibitor drugs</subject><subject>Kinases</subject><subject>Leucine Zippers</subject><subject>Leukemia</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - drug therapy</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - pathology</subject><subject>Male</subject><subject>Medical diagnosis</subject><subject>Medical prognosis</subject><subject>Oct-4 protein</subject><subject>oncogenes</subject><subject>Patients</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Sorafenib - pharmacology</subject><subject>Stem cells</subject><subject>Surgery</subject><subject>Targeted cancer therapy</subject><subject>Therapeutic applications</subject><subject>Transcription factors</subject><subject>Tumors</subject><subject>tumour markers</subject><subject>Xenografts</subject><issn>0017-5749</issn><issn>1468-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkEFPwyAYhonRuDn9Ax4MiedOKLSlR7M4p1myi54byj60s4UJdIn_XpbOeTOeCPC87_flQeiakimlLL9768PGtElKqEgYLTgnJ2hMeR5vqRCnaEwILZKs4OUIXXi_IYQIUdJzNGKUUpHyYow-VkZZDUG2eLGc4-Ck8VKFZicDeKyS597gYPHW2c4GwO-wlcEqaNu-lQ4r6VRjbCfxGnbQ2m0HJmBp1thbJzWYpsYOfOODNAou0ZmWrYerwzlBr_OHl9kiWa4en2b3y6TmBQ-JhhKYKEghKGS6LAVTXPBM14JlpOapZPGB0UyBIqXQdU4YrGXOteKy5vFrgm6H3rj1Zw8-VBvbOxNHVmkUU5RZnqeRSgdKOeu9A11tXdNJ91VRUu39VoPfau-3GvzG0M2huq87WB8jP0IjkAxA3W3-Vzj95Y9r_hH4Bg_Clmw</recordid><startdate>20191001</startdate><enddate>20191001</enddate><creator>Xiang, Dai-Min</creator><creator>Sun, Wen</creator><creator>Zhou, Tengfei</creator><creator>Zhang, Cheng</creator><creator>Cheng, Zhuo</creator><creator>Li, Shi-Chao</creator><creator>Jiang, Weiqi</creator><creator>Wang, Ruoyu</creator><creator>Fu, Gongbo</creator><creator>Cui, Xiuliang</creator><creator>Hou, Guojun</creator><creator>Jin, Guang-Zhi</creator><creator>Li, Hengyu</creator><creator>Hou, Caiying</creator><creator>Liu, Hui</creator><creator>Wang, Hongyang</creator><creator>Ding, Jin</creator><general>BMJ Publishing Group Ltd and British Society of Gastroenterology</general><general>BMJ Publishing Group LTD</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>K9.</scope><orcidid>https://orcid.org/0000-0002-4709-3334</orcidid></search><sort><creationdate>20191001</creationdate><title>Oncofetal HLF transactivates c-Jun to promote hepatocellular carcinoma development and sorafenib resistance</title><author>Xiang, Dai-Min ; Sun, Wen ; Zhou, Tengfei ; Zhang, Cheng ; Cheng, Zhuo ; Li, Shi-Chao ; Jiang, Weiqi ; Wang, Ruoyu ; Fu, Gongbo ; Cui, Xiuliang ; Hou, Guojun ; Jin, Guang-Zhi ; Li, Hengyu ; Hou, Caiying ; Liu, Hui ; Wang, Hongyang ; Ding, Jin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b474t-fe9e3870781e5f9983c4845fb8350b42a33c4315cec098fb603eda64fc4ab4c43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adult</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Basic-Leucine Zipper Transcription Factors - biosynthesis</topic><topic>Basic-Leucine Zipper Transcription Factors - genetics</topic><topic>Biomarkers</topic><topic>c-Jun protein</topic><topic>Cancer therapies</topic><topic>carcinogenesis</topic><topic>Carcinoma, Hepatocellular - drug therapy</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Cell Line, Tumor</topic><topic>Clinical medicine</topic><topic>Disease Progression</topic><topic>DNA, Neoplasm - genetics</topic><topic>drug resistance</topic><topic>Drug Resistance, Neoplasm</topic><topic>Female</topic><topic>Fetuses</topic><topic>Gene expression</topic><topic>Genes, jun - genetics</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatology</topic><topic>Hepatoma</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Inhibitor drugs</topic><topic>Kinases</topic><topic>Leucine Zippers</topic><topic>Leukemia</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - drug therapy</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - pathology</topic><topic>Male</topic><topic>Medical diagnosis</topic><topic>Medical prognosis</topic><topic>Oct-4 protein</topic><topic>oncogenes</topic><topic>Patients</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>Sorafenib - pharmacology</topic><topic>Stem cells</topic><topic>Surgery</topic><topic>Targeted cancer therapy</topic><topic>Therapeutic applications</topic><topic>Transcription factors</topic><topic>Tumors</topic><topic>tumour markers</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xiang, Dai-Min</creatorcontrib><creatorcontrib>Sun, Wen</creatorcontrib><creatorcontrib>Zhou, Tengfei</creatorcontrib><creatorcontrib>Zhang, Cheng</creatorcontrib><creatorcontrib>Cheng, Zhuo</creatorcontrib><creatorcontrib>Li, Shi-Chao</creatorcontrib><creatorcontrib>Jiang, Weiqi</creatorcontrib><creatorcontrib>Wang, Ruoyu</creatorcontrib><creatorcontrib>Fu, Gongbo</creatorcontrib><creatorcontrib>Cui, Xiuliang</creatorcontrib><creatorcontrib>Hou, Guojun</creatorcontrib><creatorcontrib>Jin, Guang-Zhi</creatorcontrib><creatorcontrib>Li, Hengyu</creatorcontrib><creatorcontrib>Hou, Caiying</creatorcontrib><creatorcontrib>Liu, Hui</creatorcontrib><creatorcontrib>Wang, Hongyang</creatorcontrib><creatorcontrib>Ding, Jin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Gut</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xiang, Dai-Min</au><au>Sun, Wen</au><au>Zhou, Tengfei</au><au>Zhang, Cheng</au><au>Cheng, Zhuo</au><au>Li, Shi-Chao</au><au>Jiang, Weiqi</au><au>Wang, Ruoyu</au><au>Fu, Gongbo</au><au>Cui, Xiuliang</au><au>Hou, Guojun</au><au>Jin, Guang-Zhi</au><au>Li, Hengyu</au><au>Hou, Caiying</au><au>Liu, Hui</au><au>Wang, Hongyang</au><au>Ding, Jin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oncofetal HLF transactivates c-Jun to promote hepatocellular carcinoma development and sorafenib resistance</atitle><jtitle>Gut</jtitle><stitle>Gut</stitle><addtitle>Gut</addtitle><date>2019-10-01</date><risdate>2019</risdate><volume>68</volume><issue>10</issue><spage>1858</spage><epage>1871</epage><pages>1858-1871</pages><issn>0017-5749</issn><eissn>1468-3288</eissn><abstract>Background and aimsThe unique expression pattern makes oncofetal proteins ideal diagnostic biomarkers and therapeutic targets in cancer. However, few oncofetal proteins have been identified and entered clinical practice.MethodsFetal liver, adult liver and hepatocellular carcinoma (HCC) tissues were employed to assess the expression of hepatic leukaemia factor (HLF). The impact of HLF on HCC onset and progression was investigated both in vivo and in vitro. The association between HLF and patient prognosis was determined in patient cohorts. The correlation between HLF expression and sorafenib benefits in HCC was further evaluated in patient cohorts and patient-derived xenografts (PDXs).ResultsHLF is a novel oncofetal protein which is reactivated in HCC by SOX2 and OCT4. Functional studies revealed that HLF transactivates c-Jun to promote tumour initiating cell (TIC) generation and enhances TIC-like properties of hepatoma cells, thus driving HCC initiation and progression. Consistently, our clinical investigations elucidated the association between HLF and patient prognosis and unravelled the close correlation between HLF levels and c-Jun expression in patient HCCs. Importantly, HLF/c-Jun axis determines the responses of hepatoma cells to sorafenib treatment, and interference of HLF abrogated c-Jun activation and enhanced sorafenib response. Analysis of patient cohorts and PDXs further suggests that HLF/c-Jun axis might serve as a biomarker for sorafenib benefits in HCC patients.ConclusionsOur findings uncovered HLF as a novel oncofetal protein and revealed the crucial role of the HLF/c-Jun axis in HCC development and sorafenib response, rendering HLF as an optimal target for the prevention and intervention of HCC.</abstract><cop>England</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>31118247</pmid><doi>10.1136/gutjnl-2018-317440</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-4709-3334</orcidid></addata></record> |
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| subjects | Adult Antineoplastic Agents - pharmacology Apoptosis Basic-Leucine Zipper Transcription Factors - biosynthesis Basic-Leucine Zipper Transcription Factors - genetics Biomarkers c-Jun protein Cancer therapies carcinogenesis Carcinoma, Hepatocellular - drug therapy Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - pathology Cell Line, Tumor Clinical medicine Disease Progression DNA, Neoplasm - genetics drug resistance Drug Resistance, Neoplasm Female Fetuses Gene expression Genes, jun - genetics Hepatocellular carcinoma Hepatology Hepatoma Hospitals Humans Immunoprecipitation Inhibitor drugs Kinases Leucine Zippers Leukemia Liver cancer Liver Neoplasms - drug therapy Liver Neoplasms - genetics Liver Neoplasms - pathology Male Medical diagnosis Medical prognosis Oct-4 protein oncogenes Patients Prognosis Proteins Signal transduction Sorafenib - pharmacology Stem cells Surgery Targeted cancer therapy Therapeutic applications Transcription factors Tumors tumour markers Xenografts |
| title | Oncofetal HLF transactivates c-Jun to promote hepatocellular carcinoma development and sorafenib resistance |
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