USP14 increases the sensitivity of retinoblastoma to cisplatin by mediating the ferroptosis
The aim of this study is to explore the function of USP14 on the sensitivity of retinoblastoma (RB) to cisplatin (DDP) and the underlying mechanism. USP14 was knockdown in Y79 cells by transfecting three siRNAs (si-USP14-1, si-USP14-2, and si-USP14-3), with si-USP14 NC as the negative control. si-US...
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| creator | Liu, Han Gan, Qiang Lai, Yongping Pan, Zhenhui Jin, Qifang Li, Jiayue Wang, Nanye Jiao, Shoufeng Chai, Yong |
| description | The aim of this study is to explore the function of USP14 on the sensitivity of retinoblastoma (RB) to cisplatin (DDP) and the underlying mechanism. USP14 was knockdown in Y79 cells by transfecting three siRNAs (si-USP14-1, si-USP14-2, and si-USP14-3), with si-USP14 NC as the negative control. si-USP14-3 was selected by results of Western blotting. The CCK-8 assay was used to detect the IC50 of Y79 cells and the growth curve. The cell cycle, cell apoptosis, and ROS level were measured by flow cytometry. The expression level of P-GP, ERCC1, survivin, GPX4, FTH1, ACSL4, NOX1, COX2, and FASN was determined by the Western blotting assay. CO-IP assay was utilized to evaluate the interaction between USP14 and FASN. The IC50 of DDP in Y79 cells and Y79/DDP cells was 7.83 µM and 24.67 µM, respectively. Compared to control and si-USP14 NC groups, increased apoptotic rate and ROS level, and arrested cell cycle in S phase were observed in USP14-knockdown Y79 cells. Compared to control and si-USP14 NC groups, increased apoptotic rate and arrested cell cycle in G0/G1 phase were observed in USP14-knockdown Y79/DDP cells. Compared to control, increased ROS level was observed in USP14-knockdown Y79/DDP cells. Compared to the si-USP14 NC groups, extremely downregulated P-GP, ERCC1, survivin, GPX4, FTH1, NOX1, COX2, and FASN were observed in USP14-knockdown Y79 cells or Y79/DDP cells, accompanied by the elevated expression of ACSL4. The interaction between USP14 and FASN was identified according to the result of CO-IP assay. By silencing USP14 in Y79 and Y79/DDP cells, levels of resistance-related proteins (P-GP, ERCC1, and survivin), ferroptosis-related proteins (FTH1 and GPX4), and lipid metabolism-related proteins (NOX1, COX2, and FASN) were dramatically reduced, accompanied by enhanced ROS level, increased apoptosis, and restrained DNA content, indicating that USP14 might suppress the DDP resistance in RB by mediating ferroptosis, which is an important target for treating RB. |
| doi_str_mv | 10.1007/s00210-024-03174-9 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11522062</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3121791882</sourcerecordid><originalsourceid>FETCH-LOGICAL-c405t-44d3381de4ed8e046bba9dec4faf2a4cd18e339575fa2633783acf55c9bcd7043</originalsourceid><addsrcrecordid>eNp9kUtvFDEQhC0EIkvgD3BAlrhwGei2PTP2CaEoPKRIIEFOHCyPp2fjaHa82N5I--_xZkN4HDjZclV97lYx9hzhNQL0bzKAQGhAqAYk9qoxD9gKlRQNGhQP2arqukFh9Al7kvM1AHTYto_ZidQaTderFft--fULKh4Wn8hlyrxcEc-05FDCTSh7HieeqIQlDrPLJW4cL5H7kLezq6982PMNjeFwX99mJ0opbkvMIT9ljyY3Z3p2d56yy_fn384-NhefP3w6e3fReAVtaZQapdQ4kqJRE6huGJwZyavJTcIpP6ImKU3bt5MTnZS9ls5PbevN4McelDxlb4_c7W6ow3haSnKz3aawcWlvowv2b2UJV3YdbyxiKwR0ohJe3RFS_LGjXOwmZE_z7BaKu2wldFJ1qgeo1pf_WK_jLi11PytRYG9Q6wNQHF0-xZwTTffTINhDefZYnq3l2dvyrKmhF3_ucR_51VY1yKMhV2lZU_r993-wPwF3oabH</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3121791882</pqid></control><display><type>article</type><title>USP14 increases the sensitivity of retinoblastoma to cisplatin by mediating the ferroptosis</title><source>SpringerLink Journals - AutoHoldings</source><creator>Liu, Han ; Gan, Qiang ; Lai, Yongping ; Pan, Zhenhui ; Jin, Qifang ; Li, Jiayue ; Wang, Nanye ; Jiao, Shoufeng ; Chai, Yong</creator><creatorcontrib>Liu, Han ; Gan, Qiang ; Lai, Yongping ; Pan, Zhenhui ; Jin, Qifang ; Li, Jiayue ; Wang, Nanye ; Jiao, Shoufeng ; Chai, Yong</creatorcontrib><description>The aim of this study is to explore the function of USP14 on the sensitivity of retinoblastoma (RB) to cisplatin (DDP) and the underlying mechanism. USP14 was knockdown in Y79 cells by transfecting three siRNAs (si-USP14-1, si-USP14-2, and si-USP14-3), with si-USP14 NC as the negative control. si-USP14-3 was selected by results of Western blotting. The CCK-8 assay was used to detect the IC50 of Y79 cells and the growth curve. The cell cycle, cell apoptosis, and ROS level were measured by flow cytometry. The expression level of P-GP, ERCC1, survivin, GPX4, FTH1, ACSL4, NOX1, COX2, and FASN was determined by the Western blotting assay. CO-IP assay was utilized to evaluate the interaction between USP14 and FASN. The IC50 of DDP in Y79 cells and Y79/DDP cells was 7.83 µM and 24.67 µM, respectively. Compared to control and si-USP14 NC groups, increased apoptotic rate and ROS level, and arrested cell cycle in S phase were observed in USP14-knockdown Y79 cells. Compared to control and si-USP14 NC groups, increased apoptotic rate and arrested cell cycle in G0/G1 phase were observed in USP14-knockdown Y79/DDP cells. Compared to control, increased ROS level was observed in USP14-knockdown Y79/DDP cells. Compared to the si-USP14 NC groups, extremely downregulated P-GP, ERCC1, survivin, GPX4, FTH1, NOX1, COX2, and FASN were observed in USP14-knockdown Y79 cells or Y79/DDP cells, accompanied by the elevated expression of ACSL4. The interaction between USP14 and FASN was identified according to the result of CO-IP assay. By silencing USP14 in Y79 and Y79/DDP cells, levels of resistance-related proteins (P-GP, ERCC1, and survivin), ferroptosis-related proteins (FTH1 and GPX4), and lipid metabolism-related proteins (NOX1, COX2, and FASN) were dramatically reduced, accompanied by enhanced ROS level, increased apoptosis, and restrained DNA content, indicating that USP14 might suppress the DDP resistance in RB by mediating ferroptosis, which is an important target for treating RB.</description><identifier>ISSN: 0028-1298</identifier><identifier>ISSN: 1432-1912</identifier><identifier>EISSN: 1432-1912</identifier><identifier>DOI: 10.1007/s00210-024-03174-9</identifier><identifier>PMID: 38819674</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Cell cycle ; Cholecystokinin ; Cisplatin ; Cyclooxygenase-2 ; ERCC1 protein ; Ferroptosis ; Flow cytometry ; G1 phase ; Lipid metabolism ; Neurosciences ; Pharmacology/Toxicology ; Proteins ; Retinoblastoma ; S phase ; siRNA ; Survivin ; Western blotting</subject><ispartof>Naunyn-Schmiedeberg's archives of pharmacology, 2024-11, Vol.397 (11), p.8671-8680</ispartof><rights>The Author(s) 2024</rights><rights>2024. The Author(s).</rights><rights>The Author(s) 2024. This work is published under http://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) 2024 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-44d3381de4ed8e046bba9dec4faf2a4cd18e339575fa2633783acf55c9bcd7043</citedby><cites>FETCH-LOGICAL-c405t-44d3381de4ed8e046bba9dec4faf2a4cd18e339575fa2633783acf55c9bcd7043</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00210-024-03174-9$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00210-024-03174-9$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38819674$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Han</creatorcontrib><creatorcontrib>Gan, Qiang</creatorcontrib><creatorcontrib>Lai, Yongping</creatorcontrib><creatorcontrib>Pan, Zhenhui</creatorcontrib><creatorcontrib>Jin, Qifang</creatorcontrib><creatorcontrib>Li, Jiayue</creatorcontrib><creatorcontrib>Wang, Nanye</creatorcontrib><creatorcontrib>Jiao, Shoufeng</creatorcontrib><creatorcontrib>Chai, Yong</creatorcontrib><title>USP14 increases the sensitivity of retinoblastoma to cisplatin by mediating the ferroptosis</title><title>Naunyn-Schmiedeberg's archives of pharmacology</title><addtitle>Naunyn-Schmiedeberg's Arch Pharmacol</addtitle><addtitle>Naunyn Schmiedebergs Arch Pharmacol</addtitle><description>The aim of this study is to explore the function of USP14 on the sensitivity of retinoblastoma (RB) to cisplatin (DDP) and the underlying mechanism. USP14 was knockdown in Y79 cells by transfecting three siRNAs (si-USP14-1, si-USP14-2, and si-USP14-3), with si-USP14 NC as the negative control. si-USP14-3 was selected by results of Western blotting. The CCK-8 assay was used to detect the IC50 of Y79 cells and the growth curve. The cell cycle, cell apoptosis, and ROS level were measured by flow cytometry. The expression level of P-GP, ERCC1, survivin, GPX4, FTH1, ACSL4, NOX1, COX2, and FASN was determined by the Western blotting assay. CO-IP assay was utilized to evaluate the interaction between USP14 and FASN. The IC50 of DDP in Y79 cells and Y79/DDP cells was 7.83 µM and 24.67 µM, respectively. Compared to control and si-USP14 NC groups, increased apoptotic rate and ROS level, and arrested cell cycle in S phase were observed in USP14-knockdown Y79 cells. Compared to control and si-USP14 NC groups, increased apoptotic rate and arrested cell cycle in G0/G1 phase were observed in USP14-knockdown Y79/DDP cells. Compared to control, increased ROS level was observed in USP14-knockdown Y79/DDP cells. Compared to the si-USP14 NC groups, extremely downregulated P-GP, ERCC1, survivin, GPX4, FTH1, NOX1, COX2, and FASN were observed in USP14-knockdown Y79 cells or Y79/DDP cells, accompanied by the elevated expression of ACSL4. The interaction between USP14 and FASN was identified according to the result of CO-IP assay. By silencing USP14 in Y79 and Y79/DDP cells, levels of resistance-related proteins (P-GP, ERCC1, and survivin), ferroptosis-related proteins (FTH1 and GPX4), and lipid metabolism-related proteins (NOX1, COX2, and FASN) were dramatically reduced, accompanied by enhanced ROS level, increased apoptosis, and restrained DNA content, indicating that USP14 might suppress the DDP resistance in RB by mediating ferroptosis, which is an important target for treating RB.</description><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell cycle</subject><subject>Cholecystokinin</subject><subject>Cisplatin</subject><subject>Cyclooxygenase-2</subject><subject>ERCC1 protein</subject><subject>Ferroptosis</subject><subject>Flow cytometry</subject><subject>G1 phase</subject><subject>Lipid metabolism</subject><subject>Neurosciences</subject><subject>Pharmacology/Toxicology</subject><subject>Proteins</subject><subject>Retinoblastoma</subject><subject>S phase</subject><subject>siRNA</subject><subject>Survivin</subject><subject>Western blotting</subject><issn>0028-1298</issn><issn>1432-1912</issn><issn>1432-1912</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><recordid>eNp9kUtvFDEQhC0EIkvgD3BAlrhwGei2PTP2CaEoPKRIIEFOHCyPp2fjaHa82N5I--_xZkN4HDjZclV97lYx9hzhNQL0bzKAQGhAqAYk9qoxD9gKlRQNGhQP2arqukFh9Al7kvM1AHTYto_ZidQaTderFft--fULKh4Wn8hlyrxcEc-05FDCTSh7HieeqIQlDrPLJW4cL5H7kLezq6982PMNjeFwX99mJ0opbkvMIT9ljyY3Z3p2d56yy_fn384-NhefP3w6e3fReAVtaZQapdQ4kqJRE6huGJwZyavJTcIpP6ImKU3bt5MTnZS9ls5PbevN4McelDxlb4_c7W6ow3haSnKz3aawcWlvowv2b2UJV3YdbyxiKwR0ohJe3RFS_LGjXOwmZE_z7BaKu2wldFJ1qgeo1pf_WK_jLi11PytRYG9Q6wNQHF0-xZwTTffTINhDefZYnq3l2dvyrKmhF3_ucR_51VY1yKMhV2lZU_r993-wPwF3oabH</recordid><startdate>20241101</startdate><enddate>20241101</enddate><creator>Liu, Han</creator><creator>Gan, Qiang</creator><creator>Lai, Yongping</creator><creator>Pan, Zhenhui</creator><creator>Jin, Qifang</creator><creator>Li, Jiayue</creator><creator>Wang, Nanye</creator><creator>Jiao, Shoufeng</creator><creator>Chai, Yong</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20241101</creationdate><title>USP14 increases the sensitivity of retinoblastoma to cisplatin by mediating the ferroptosis</title><author>Liu, Han ; Gan, Qiang ; Lai, Yongping ; Pan, Zhenhui ; Jin, Qifang ; Li, Jiayue ; Wang, Nanye ; Jiao, Shoufeng ; Chai, Yong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-44d3381de4ed8e046bba9dec4faf2a4cd18e339575fa2633783acf55c9bcd7043</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell cycle</topic><topic>Cholecystokinin</topic><topic>Cisplatin</topic><topic>Cyclooxygenase-2</topic><topic>ERCC1 protein</topic><topic>Ferroptosis</topic><topic>Flow cytometry</topic><topic>G1 phase</topic><topic>Lipid metabolism</topic><topic>Neurosciences</topic><topic>Pharmacology/Toxicology</topic><topic>Proteins</topic><topic>Retinoblastoma</topic><topic>S phase</topic><topic>siRNA</topic><topic>Survivin</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Han</creatorcontrib><creatorcontrib>Gan, Qiang</creatorcontrib><creatorcontrib>Lai, Yongping</creatorcontrib><creatorcontrib>Pan, Zhenhui</creatorcontrib><creatorcontrib>Jin, Qifang</creatorcontrib><creatorcontrib>Li, Jiayue</creatorcontrib><creatorcontrib>Wang, Nanye</creatorcontrib><creatorcontrib>Jiao, Shoufeng</creatorcontrib><creatorcontrib>Chai, Yong</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Naunyn-Schmiedeberg's archives of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Han</au><au>Gan, Qiang</au><au>Lai, Yongping</au><au>Pan, Zhenhui</au><au>Jin, Qifang</au><au>Li, Jiayue</au><au>Wang, Nanye</au><au>Jiao, Shoufeng</au><au>Chai, Yong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>USP14 increases the sensitivity of retinoblastoma to cisplatin by mediating the ferroptosis</atitle><jtitle>Naunyn-Schmiedeberg's archives of pharmacology</jtitle><stitle>Naunyn-Schmiedeberg's Arch Pharmacol</stitle><addtitle>Naunyn Schmiedebergs Arch Pharmacol</addtitle><date>2024-11-01</date><risdate>2024</risdate><volume>397</volume><issue>11</issue><spage>8671</spage><epage>8680</epage><pages>8671-8680</pages><issn>0028-1298</issn><issn>1432-1912</issn><eissn>1432-1912</eissn><abstract>The aim of this study is to explore the function of USP14 on the sensitivity of retinoblastoma (RB) to cisplatin (DDP) and the underlying mechanism. USP14 was knockdown in Y79 cells by transfecting three siRNAs (si-USP14-1, si-USP14-2, and si-USP14-3), with si-USP14 NC as the negative control. si-USP14-3 was selected by results of Western blotting. The CCK-8 assay was used to detect the IC50 of Y79 cells and the growth curve. The cell cycle, cell apoptosis, and ROS level were measured by flow cytometry. The expression level of P-GP, ERCC1, survivin, GPX4, FTH1, ACSL4, NOX1, COX2, and FASN was determined by the Western blotting assay. CO-IP assay was utilized to evaluate the interaction between USP14 and FASN. The IC50 of DDP in Y79 cells and Y79/DDP cells was 7.83 µM and 24.67 µM, respectively. Compared to control and si-USP14 NC groups, increased apoptotic rate and ROS level, and arrested cell cycle in S phase were observed in USP14-knockdown Y79 cells. Compared to control and si-USP14 NC groups, increased apoptotic rate and arrested cell cycle in G0/G1 phase were observed in USP14-knockdown Y79/DDP cells. Compared to control, increased ROS level was observed in USP14-knockdown Y79/DDP cells. Compared to the si-USP14 NC groups, extremely downregulated P-GP, ERCC1, survivin, GPX4, FTH1, NOX1, COX2, and FASN were observed in USP14-knockdown Y79 cells or Y79/DDP cells, accompanied by the elevated expression of ACSL4. The interaction between USP14 and FASN was identified according to the result of CO-IP assay. By silencing USP14 in Y79 and Y79/DDP cells, levels of resistance-related proteins (P-GP, ERCC1, and survivin), ferroptosis-related proteins (FTH1 and GPX4), and lipid metabolism-related proteins (NOX1, COX2, and FASN) were dramatically reduced, accompanied by enhanced ROS level, increased apoptosis, and restrained DNA content, indicating that USP14 might suppress the DDP resistance in RB by mediating ferroptosis, which is an important target for treating RB.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>38819674</pmid><doi>10.1007/s00210-024-03174-9</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Biomedical and Life Sciences Biomedicine Cell cycle Cholecystokinin Cisplatin Cyclooxygenase-2 ERCC1 protein Ferroptosis Flow cytometry G1 phase Lipid metabolism Neurosciences Pharmacology/Toxicology Proteins Retinoblastoma S phase siRNA Survivin Western blotting |
| title | USP14 increases the sensitivity of retinoblastoma to cisplatin by mediating the ferroptosis |
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