Receptor interactive protein kinase 3 promotes Cisplatin-triggered necrosis in apoptosis-resistant esophageal squamous cell carcinoma cells
Cisplatin-based chemotherapy is currently the standard treatment for locally advanced esophageal cancer. Cisplatin has been shown to induce both apoptosis and necrosis in cancer cells, but the mechanism by which programmed necrosis is induced remains unknown. In this study, we provide evidence that...
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| description | Cisplatin-based chemotherapy is currently the standard treatment for locally advanced esophageal cancer. Cisplatin has been shown to induce both apoptosis and necrosis in cancer cells, but the mechanism by which programmed necrosis is induced remains unknown. In this study, we provide evidence that cisplatin induces necrotic cell death in apoptosis-resistant esophageal cancer cells. This cell death is dependent on RIPK3 and on necrosome formation via autocrine production of TNFα. More importantly, we demonstrate that RIPK3 is necessary for cisplatin-induced killing of esophageal cancer cells because inhibition of RIPK1 activity by necrostatin or knockdown of RIPK3 significantly attenuates necrosis and leads to cisplatin resistance. Moreover, microarray analysis confirmed an anti-apoptotic molecular expression pattern in esophageal cancer cells in response to cisplatin. Taken together, our data indicate that RIPK3 and autocrine production of TNFα contribute to cisplatin sensitivity by initiating necrosis when the apoptotic pathway is suppressed or absent in esophageal cancer cells. These data provide new insight into the molecular mechanisms underlying cisplatin-induced necrosis and suggest that RIPK3 is a potential marker for predicting cisplatin sensitivity in apoptosis-resistant and advanced esophageal cancer. |
| doi_str_mv | 10.1371/journal.pone.0100127 |
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Cisplatin has been shown to induce both apoptosis and necrosis in cancer cells, but the mechanism by which programmed necrosis is induced remains unknown. In this study, we provide evidence that cisplatin induces necrotic cell death in apoptosis-resistant esophageal cancer cells. This cell death is dependent on RIPK3 and on necrosome formation via autocrine production of TNFα. More importantly, we demonstrate that RIPK3 is necessary for cisplatin-induced killing of esophageal cancer cells because inhibition of RIPK1 activity by necrostatin or knockdown of RIPK3 significantly attenuates necrosis and leads to cisplatin resistance. Moreover, microarray analysis confirmed an anti-apoptotic molecular expression pattern in esophageal cancer cells in response to cisplatin. Taken together, our data indicate that RIPK3 and autocrine production of TNFα contribute to cisplatin sensitivity by initiating necrosis when the apoptotic pathway is suppressed or absent in esophageal cancer cells. These data provide new insight into the molecular mechanisms underlying cisplatin-induced necrosis and suggest that RIPK3 is a potential marker for predicting cisplatin sensitivity in apoptosis-resistant and advanced esophageal cancer.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0100127</identifier><identifier>PMID: 24959694</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Antineoplastic Agents - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; Autocrine signalling ; Cancer ; Cancer therapies ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - metabolism ; Carcinoma, Squamous Cell - pathology ; Cell death ; Cell Line, Tumor ; Chemotherapy ; Cisplatin ; Cisplatin - pharmacology ; Disease Models, Animal ; Esophageal cancer ; Esophageal Neoplasms - genetics ; Esophageal Neoplasms - metabolism ; Esophageal Neoplasms - pathology ; Esophageal Squamous Cell Carcinoma ; Esophagus ; Gene Expression Regulation, Neoplastic - drug effects ; Gene Knockout Techniques ; Hospitals ; Humans ; Intracellular Signaling Peptides and Proteins - deficiency ; Kinases ; Laboratories ; Medicine and Health Sciences ; Mice ; Mitochondrial Proteins - deficiency ; Molecular modelling ; Necrosis ; Necrosis - chemically induced ; Necrosis - genetics ; Oncology ; Protein kinase ; Proteins ; Radiation therapy ; Receptor-Interacting Protein Serine-Threonine Kinases - genetics ; Receptor-Interacting Protein Serine-Threonine Kinases - metabolism ; RNA Interference ; Sensitivity ; Signal Transduction ; Squamous cell carcinoma ; Tumor Burden - drug effects ; Tumor Burden - genetics ; Tumor Necrosis Factor-alpha - biosynthesis ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Xenograft Model Antitumor Assays</subject><ispartof>PloS one, 2014-06, Vol.9 (6), p.e100127</ispartof><rights>2014 Xu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Xu et al 2014 Xu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c592t-f97524d4ecb9b0a1c566a4646756d752d1254441d40f8d5fdf849458ebab8df63</citedby><cites>FETCH-LOGICAL-c592t-f97524d4ecb9b0a1c566a4646756d752d1254441d40f8d5fdf849458ebab8df63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4069059/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4069059/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24959694$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Yang</creatorcontrib><creatorcontrib>Lin, Zhengwei</creatorcontrib><creatorcontrib>Zhao, Nan</creatorcontrib><creatorcontrib>Zhou, Lanping</creatorcontrib><creatorcontrib>Liu, Fang</creatorcontrib><creatorcontrib>Cichacz, Zbigniew</creatorcontrib><creatorcontrib>Zhang, Lin</creatorcontrib><creatorcontrib>Zhan, Qimin</creatorcontrib><creatorcontrib>Zhao, Xiaohang</creatorcontrib><title>Receptor interactive protein kinase 3 promotes Cisplatin-triggered necrosis in apoptosis-resistant esophageal squamous cell carcinoma cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Cisplatin-based chemotherapy is currently the standard treatment for locally advanced esophageal cancer. Cisplatin has been shown to induce both apoptosis and necrosis in cancer cells, but the mechanism by which programmed necrosis is induced remains unknown. In this study, we provide evidence that cisplatin induces necrotic cell death in apoptosis-resistant esophageal cancer cells. This cell death is dependent on RIPK3 and on necrosome formation via autocrine production of TNFα. More importantly, we demonstrate that RIPK3 is necessary for cisplatin-induced killing of esophageal cancer cells because inhibition of RIPK1 activity by necrostatin or knockdown of RIPK3 significantly attenuates necrosis and leads to cisplatin resistance. Moreover, microarray analysis confirmed an anti-apoptotic molecular expression pattern in esophageal cancer cells in response to cisplatin. Taken together, our data indicate that RIPK3 and autocrine production of TNFα contribute to cisplatin sensitivity by initiating necrosis when the apoptotic pathway is suppressed or absent in esophageal cancer cells. These data provide new insight into the molecular mechanisms underlying cisplatin-induced necrosis and suggest that RIPK3 is a potential marker for predicting cisplatin sensitivity in apoptosis-resistant and advanced esophageal cancer.</description><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Autocrine signalling</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell death</subject><subject>Cell Line, Tumor</subject><subject>Chemotherapy</subject><subject>Cisplatin</subject><subject>Cisplatin - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Esophageal cancer</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophageal Neoplasms - 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metabolism</subject><subject>RNA Interference</subject><subject>Sensitivity</subject><subject>Signal Transduction</subject><subject>Squamous cell carcinoma</subject><subject>Tumor Burden - drug effects</subject><subject>Tumor Burden - genetics</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNp1kltrFDEUxwdR7EW_geiAz7Mmk8tOXgRZ1BYKguhzOJOcbLPOJtMkW-hn8Eub7W5L--BLknP7nUPOv2neUbKgbEk_beIuBZgWcwy4IJQQ2i9fNKdUsb6TPWEvn7xPmrOcN4QINkj5ujnpuRJKKn7a_P2JBucSU-tDwQSm-Fts5xQL-tD-8QEytmzv2FZXblc-zxMUH7qS_HqNCW0b0KSYfa6IFuZYadXoEtazQCgt5jhfwxphavPNDrZxl1uD09QaSMaHuIV7M79pXjmYMr493ufN729ff60uuqsf3y9XX646I1RfOqeWoueWoxnVSIAaISVwyeVSSFtDlvaCc04tJ26wwlk3cMXFgCOMg3WSnTcfDtx5ilkf_zFrKlgl02Hoa8blIcNG2Og5-S2kOx3B63tHTGsNqXgzoWaK9soAMDc6Xneg2IDgmB166lAaW1mfj9124xatwVASTM-gzyPBX-t1vNWcSEWEqoCPR0CKNzvM5T8j80PWfhc5oXvsQIneC-ahSu8Fo4-CqWXvn073WPSgEPYP127Dww</recordid><startdate>20140624</startdate><enddate>20140624</enddate><creator>Xu, Yang</creator><creator>Lin, Zhengwei</creator><creator>Zhao, Nan</creator><creator>Zhou, Lanping</creator><creator>Liu, Fang</creator><creator>Cichacz, Zbigniew</creator><creator>Zhang, Lin</creator><creator>Zhan, Qimin</creator><creator>Zhao, Xiaohang</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140624</creationdate><title>Receptor interactive protein kinase 3 promotes Cisplatin-triggered necrosis in apoptosis-resistant esophageal squamous cell carcinoma cells</title><author>Xu, Yang ; Lin, Zhengwei ; Zhao, Nan ; Zhou, Lanping ; Liu, Fang ; Cichacz, Zbigniew ; Zhang, Lin ; Zhan, Qimin ; Zhao, Xiaohang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c592t-f97524d4ecb9b0a1c566a4646756d752d1254441d40f8d5fdf849458ebab8df63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - 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Cisplatin has been shown to induce both apoptosis and necrosis in cancer cells, but the mechanism by which programmed necrosis is induced remains unknown. In this study, we provide evidence that cisplatin induces necrotic cell death in apoptosis-resistant esophageal cancer cells. This cell death is dependent on RIPK3 and on necrosome formation via autocrine production of TNFα. More importantly, we demonstrate that RIPK3 is necessary for cisplatin-induced killing of esophageal cancer cells because inhibition of RIPK1 activity by necrostatin or knockdown of RIPK3 significantly attenuates necrosis and leads to cisplatin resistance. Moreover, microarray analysis confirmed an anti-apoptotic molecular expression pattern in esophageal cancer cells in response to cisplatin. Taken together, our data indicate that RIPK3 and autocrine production of TNFα contribute to cisplatin sensitivity by initiating necrosis when the apoptotic pathway is suppressed or absent in esophageal cancer cells. These data provide new insight into the molecular mechanisms underlying cisplatin-induced necrosis and suggest that RIPK3 is a potential marker for predicting cisplatin sensitivity in apoptosis-resistant and advanced esophageal cancer.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24959694</pmid><doi>10.1371/journal.pone.0100127</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Apoptosis - genetics Autocrine signalling Cancer Cancer therapies Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - pathology Cell death Cell Line, Tumor Chemotherapy Cisplatin Cisplatin - pharmacology Disease Models, Animal Esophageal cancer Esophageal Neoplasms - genetics Esophageal Neoplasms - metabolism Esophageal Neoplasms - pathology Esophageal Squamous Cell Carcinoma Esophagus Gene Expression Regulation, Neoplastic - drug effects Gene Knockout Techniques Hospitals Humans Intracellular Signaling Peptides and Proteins - deficiency Kinases Laboratories Medicine and Health Sciences Mice Mitochondrial Proteins - deficiency Molecular modelling Necrosis Necrosis - chemically induced Necrosis - genetics Oncology Protein kinase Proteins Radiation therapy Receptor-Interacting Protein Serine-Threonine Kinases - genetics Receptor-Interacting Protein Serine-Threonine Kinases - metabolism RNA Interference Sensitivity Signal Transduction Squamous cell carcinoma Tumor Burden - drug effects Tumor Burden - genetics Tumor Necrosis Factor-alpha - biosynthesis Tumor necrosis factor-TNF Tumor necrosis factor-α Xenograft Model Antitumor Assays |
| title | Receptor interactive protein kinase 3 promotes Cisplatin-triggered necrosis in apoptosis-resistant esophageal squamous cell carcinoma cells |
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