Inhibition of JNK/c-Jun-ATF2 Overcomes Cisplatin Resistance in Liver Cancer through down-Regulating Galectin-1
Due to drug resistance, the clinical response to cisplatin (CDDP) from patients with liver cancer is unsatisfactory. The alleviation or overcoming of CDDP resistance is an urgent problem to be solved in clinics. Tumor cells rapidly change signal pathways to mediate drug resistance under drug exposur...
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| Veröffentlicht in: | International journal of biological sciences 2023-01, Vol.19 (8), p.2366-2381 |
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| creator | Yang, Fan Li, Mengzhu Xu, Duo Jiang, Zebo Jiang, Hailong Xiao, Yitai Mei, Chaoming Yang, Meilin Chen, Congmin Zhou, Bin He, Bailiang Shan, Hong Pang, Pengfei Li, Dan |
| description | Due to drug resistance, the clinical response to cisplatin (CDDP) from patients with liver cancer is unsatisfactory. The alleviation or overcoming of CDDP resistance is an urgent problem to be solved in clinics. Tumor cells rapidly change signal pathways to mediate drug resistance under drug exposure. Here, multiple phosphor-kinase assays were performed and c-Jun N-terminal kinase (JNK) was activated in liver cancer cells treated with CDDP. The high activity of the JNK promotes poor progression and mediates cisplatin resistance in liver cancer, leading to a poor prognosis of liver cancer. Mechanistically, the highly activated JNK phosphorylated c-Jun and ATF2 formed a heterodimer to upregulate the expression of Galectin-1, leading to promoting cisplatin resistance in liver cancer. Importantly, we simulated the clinical evolution of drug resistance in liver cancer by continuous CDDP administration
.
bioluminescence imaging showed the activity of JNK gradually increased during this process. Moreover, the inhibition of JNK activity by small molecular or genetic inhibitors enhanced DNA damage and overcame CDDP resistance
and
Collectively, our results underline that the high activity of JNK/c-Jun-ATF2/Galectin-1 mediates cisplatin resistance in liver cancer and provides an optional scheme for dynamic monitoring of molecular activity
. |
| doi_str_mv | 10.7150/ijbs.79163 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10197891</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2816756950</sourcerecordid><originalsourceid>FETCH-LOGICAL-c407t-7b792d5dd27437e831c6077ca7964aaa0e4c96feed3d0b2a67b5baefdbd795753</originalsourceid><addsrcrecordid>eNpdkVtLxDAQhYMo3l_8ARLwRYRqkjZN8ySyeF8URJ9Dmkx3s3STNWkV_71db6hPM8N8czjDQWiPkmNBOTlxszodC0nLfAVt0qKQGWNVtfqr30BbKc0IyUtekXW0kQtGuZR0E_lrP3W161zwODT45u72xGQ3vc_OHi8Yvn-BaMIcEh65tGh15zx-gORSp70BPExjNyB4tBwj7qYx9JMptuHVZw8w6T8uJvhSt2CGLqM7aK3RbYLdr7qNni7OH0dX2fj-8np0Ns5MQUSXiVpIZrm1TBS5gCqnpiRCGC1kWWitCRRGlg2AzS2pmS5FzWsNja2tkFzwfBudfuou-noO1oDvom7VIrq5jm8qaKf-brybqkl4UZRQKSpJB4XDL4UYnntInZq7ZKBttYfQJ8UqWhHOC1YM6ME_dBb66If_llQpeCk5GaijT8rEkFKE5scNJWqZo1rmqD5yHOD93_5_0O_g8nd2zJn4</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2816756950</pqid></control><display><type>article</type><title>Inhibition of JNK/c-Jun-ATF2 Overcomes Cisplatin Resistance in Liver Cancer through down-Regulating Galectin-1</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>PubMed Central Open Access</source><creator>Yang, Fan ; Li, Mengzhu ; Xu, Duo ; Jiang, Zebo ; Jiang, Hailong ; Xiao, Yitai ; Mei, Chaoming ; Yang, Meilin ; Chen, Congmin ; Zhou, Bin ; He, Bailiang ; Shan, Hong ; Pang, Pengfei ; Li, Dan</creator><creatorcontrib>Yang, Fan ; Li, Mengzhu ; Xu, Duo ; Jiang, Zebo ; Jiang, Hailong ; Xiao, Yitai ; Mei, Chaoming ; Yang, Meilin ; Chen, Congmin ; Zhou, Bin ; He, Bailiang ; Shan, Hong ; Pang, Pengfei ; Li, Dan</creatorcontrib><description>Due to drug resistance, the clinical response to cisplatin (CDDP) from patients with liver cancer is unsatisfactory. The alleviation or overcoming of CDDP resistance is an urgent problem to be solved in clinics. Tumor cells rapidly change signal pathways to mediate drug resistance under drug exposure. Here, multiple phosphor-kinase assays were performed and c-Jun N-terminal kinase (JNK) was activated in liver cancer cells treated with CDDP. The high activity of the JNK promotes poor progression and mediates cisplatin resistance in liver cancer, leading to a poor prognosis of liver cancer. Mechanistically, the highly activated JNK phosphorylated c-Jun and ATF2 formed a heterodimer to upregulate the expression of Galectin-1, leading to promoting cisplatin resistance in liver cancer. Importantly, we simulated the clinical evolution of drug resistance in liver cancer by continuous CDDP administration
.
bioluminescence imaging showed the activity of JNK gradually increased during this process. Moreover, the inhibition of JNK activity by small molecular or genetic inhibitors enhanced DNA damage and overcame CDDP resistance
and
Collectively, our results underline that the high activity of JNK/c-Jun-ATF2/Galectin-1 mediates cisplatin resistance in liver cancer and provides an optional scheme for dynamic monitoring of molecular activity
.</description><identifier>ISSN: 1449-2288</identifier><identifier>EISSN: 1449-2288</identifier><identifier>DOI: 10.7150/ijbs.79163</identifier><identifier>PMID: 37215991</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>Activating Transcription Factor 2 - genetics ; Activating Transcription Factor 2 - metabolism ; Antibodies ; Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Apoptosis ; Bioluminescence ; c-Jun protein ; Cancer therapies ; Cell Line, Tumor ; Cells ; Chemotherapy ; Cisplatin ; Cisplatin - pharmacology ; Cisplatin - therapeutic use ; Colorectal cancer ; DNA damage ; Drug resistance ; Drug Resistance, Neoplasm - genetics ; Galectin 1 - genetics ; Galectin-1 ; Hepatocytes ; Humans ; JNK Mitogen-Activated Protein Kinases - metabolism ; JNK protein ; Kinases ; Liver cancer ; Liver Neoplasms - drug therapy ; Liver Neoplasms - genetics ; Medical prognosis ; Membranes ; Phosphors ; Plasmids ; Proteins ; Research Paper ; Transcription factors ; Tumor cells</subject><ispartof>International journal of biological sciences, 2023-01, Vol.19 (8), p.2366-2381</ispartof><rights>The author(s).</rights><rights>2023. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The author(s) 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c407t-7b792d5dd27437e831c6077ca7964aaa0e4c96feed3d0b2a67b5baefdbd795753</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10197891/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10197891/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37215991$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Fan</creatorcontrib><creatorcontrib>Li, Mengzhu</creatorcontrib><creatorcontrib>Xu, Duo</creatorcontrib><creatorcontrib>Jiang, Zebo</creatorcontrib><creatorcontrib>Jiang, Hailong</creatorcontrib><creatorcontrib>Xiao, Yitai</creatorcontrib><creatorcontrib>Mei, Chaoming</creatorcontrib><creatorcontrib>Yang, Meilin</creatorcontrib><creatorcontrib>Chen, Congmin</creatorcontrib><creatorcontrib>Zhou, Bin</creatorcontrib><creatorcontrib>He, Bailiang</creatorcontrib><creatorcontrib>Shan, Hong</creatorcontrib><creatorcontrib>Pang, Pengfei</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><title>Inhibition of JNK/c-Jun-ATF2 Overcomes Cisplatin Resistance in Liver Cancer through down-Regulating Galectin-1</title><title>International journal of biological sciences</title><addtitle>Int J Biol Sci</addtitle><description>Due to drug resistance, the clinical response to cisplatin (CDDP) from patients with liver cancer is unsatisfactory. The alleviation or overcoming of CDDP resistance is an urgent problem to be solved in clinics. Tumor cells rapidly change signal pathways to mediate drug resistance under drug exposure. Here, multiple phosphor-kinase assays were performed and c-Jun N-terminal kinase (JNK) was activated in liver cancer cells treated with CDDP. The high activity of the JNK promotes poor progression and mediates cisplatin resistance in liver cancer, leading to a poor prognosis of liver cancer. Mechanistically, the highly activated JNK phosphorylated c-Jun and ATF2 formed a heterodimer to upregulate the expression of Galectin-1, leading to promoting cisplatin resistance in liver cancer. Importantly, we simulated the clinical evolution of drug resistance in liver cancer by continuous CDDP administration
.
bioluminescence imaging showed the activity of JNK gradually increased during this process. Moreover, the inhibition of JNK activity by small molecular or genetic inhibitors enhanced DNA damage and overcame CDDP resistance
and
Collectively, our results underline that the high activity of JNK/c-Jun-ATF2/Galectin-1 mediates cisplatin resistance in liver cancer and provides an optional scheme for dynamic monitoring of molecular activity
.</description><subject>Activating Transcription Factor 2 - genetics</subject><subject>Activating Transcription Factor 2 - metabolism</subject><subject>Antibodies</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Apoptosis</subject><subject>Bioluminescence</subject><subject>c-Jun protein</subject><subject>Cancer therapies</subject><subject>Cell Line, Tumor</subject><subject>Cells</subject><subject>Chemotherapy</subject><subject>Cisplatin</subject><subject>Cisplatin - pharmacology</subject><subject>Cisplatin - therapeutic use</subject><subject>Colorectal cancer</subject><subject>DNA damage</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Galectin 1 - genetics</subject><subject>Galectin-1</subject><subject>Hepatocytes</subject><subject>Humans</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>JNK protein</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - drug therapy</subject><subject>Liver Neoplasms - genetics</subject><subject>Medical prognosis</subject><subject>Membranes</subject><subject>Phosphors</subject><subject>Plasmids</subject><subject>Proteins</subject><subject>Research Paper</subject><subject>Transcription factors</subject><subject>Tumor cells</subject><issn>1449-2288</issn><issn>1449-2288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkVtLxDAQhYMo3l_8ARLwRYRqkjZN8ySyeF8URJ9Dmkx3s3STNWkV_71db6hPM8N8czjDQWiPkmNBOTlxszodC0nLfAVt0qKQGWNVtfqr30BbKc0IyUtekXW0kQtGuZR0E_lrP3W161zwODT45u72xGQ3vc_OHi8Yvn-BaMIcEh65tGh15zx-gORSp70BPExjNyB4tBwj7qYx9JMptuHVZw8w6T8uJvhSt2CGLqM7aK3RbYLdr7qNni7OH0dX2fj-8np0Ns5MQUSXiVpIZrm1TBS5gCqnpiRCGC1kWWitCRRGlg2AzS2pmS5FzWsNja2tkFzwfBudfuou-noO1oDvom7VIrq5jm8qaKf-brybqkl4UZRQKSpJB4XDL4UYnntInZq7ZKBttYfQJ8UqWhHOC1YM6ME_dBb66If_llQpeCk5GaijT8rEkFKE5scNJWqZo1rmqD5yHOD93_5_0O_g8nd2zJn4</recordid><startdate>20230101</startdate><enddate>20230101</enddate><creator>Yang, Fan</creator><creator>Li, Mengzhu</creator><creator>Xu, Duo</creator><creator>Jiang, Zebo</creator><creator>Jiang, Hailong</creator><creator>Xiao, Yitai</creator><creator>Mei, Chaoming</creator><creator>Yang, Meilin</creator><creator>Chen, Congmin</creator><creator>Zhou, Bin</creator><creator>He, Bailiang</creator><creator>Shan, Hong</creator><creator>Pang, Pengfei</creator><creator>Li, Dan</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</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>7QL</scope><scope>7QO</scope><scope>7U9</scope><scope>8FD</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20230101</creationdate><title>Inhibition of JNK/c-Jun-ATF2 Overcomes Cisplatin Resistance in Liver Cancer through down-Regulating Galectin-1</title><author>Yang, Fan ; 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The alleviation or overcoming of CDDP resistance is an urgent problem to be solved in clinics. Tumor cells rapidly change signal pathways to mediate drug resistance under drug exposure. Here, multiple phosphor-kinase assays were performed and c-Jun N-terminal kinase (JNK) was activated in liver cancer cells treated with CDDP. The high activity of the JNK promotes poor progression and mediates cisplatin resistance in liver cancer, leading to a poor prognosis of liver cancer. Mechanistically, the highly activated JNK phosphorylated c-Jun and ATF2 formed a heterodimer to upregulate the expression of Galectin-1, leading to promoting cisplatin resistance in liver cancer. Importantly, we simulated the clinical evolution of drug resistance in liver cancer by continuous CDDP administration
.
bioluminescence imaging showed the activity of JNK gradually increased during this process. Moreover, the inhibition of JNK activity by small molecular or genetic inhibitors enhanced DNA damage and overcame CDDP resistance
and
Collectively, our results underline that the high activity of JNK/c-Jun-ATF2/Galectin-1 mediates cisplatin resistance in liver cancer and provides an optional scheme for dynamic monitoring of molecular activity
.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>37215991</pmid><doi>10.7150/ijbs.79163</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Activating Transcription Factor 2 - genetics Activating Transcription Factor 2 - metabolism Antibodies Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Apoptosis Bioluminescence c-Jun protein Cancer therapies Cell Line, Tumor Cells Chemotherapy Cisplatin Cisplatin - pharmacology Cisplatin - therapeutic use Colorectal cancer DNA damage Drug resistance Drug Resistance, Neoplasm - genetics Galectin 1 - genetics Galectin-1 Hepatocytes Humans JNK Mitogen-Activated Protein Kinases - metabolism JNK protein Kinases Liver cancer Liver Neoplasms - drug therapy Liver Neoplasms - genetics Medical prognosis Membranes Phosphors Plasmids Proteins Research Paper Transcription factors Tumor cells |
| title | Inhibition of JNK/c-Jun-ATF2 Overcomes Cisplatin Resistance in Liver Cancer through down-Regulating Galectin-1 |
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