Emodin induced necroptosis in the glioma cell line U251 via the TNF-α/RIP1/RIP3 pathway
Summary Emodin, an anthraquinone compound extracted from rhubarb and other traditional Chinese medicines, has been proven to have a wide range of pharmacological effects, such as anti-inflammatory, antiviral, and antitumor activities. Previous studies have confirmed that emodin has inhibitory effect...
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| creator | Zhou, Jiabin Li, Genhua Han, Guangkui Feng, Song Liu, Yuhan Chen, Jun Liu, Chen Zhao, Lei Jin, Feng |
| description | Summary
Emodin, an anthraquinone compound extracted from rhubarb and other traditional Chinese medicines, has been proven to have a wide range of pharmacological effects, such as anti-inflammatory, antiviral, and antitumor activities. Previous studies have confirmed that emodin has inhibitory effects on various solid tumors, such as osteosarcoma, liver cancer, prostate cancer and glioma. This study aimed to investigate the effects and mechanisms of emodin-induced necroptosis in the glioma cell line U251 by targeting the TNF-α/RIP1/RIP3 signaling pathway. We found that emodin could significantly inhibit U251 cell proliferation, and the viability of U251 cells treated with emodin was reduced in a dose- and time-dependent manner. Flow cytometry assays and Hoechst-PI staining assays showed that emodin induced apoptosis and necroptosis. Real-time PCR and western blot analysis showed that emodin upregulated the levels of TNF-α, RIP1, RIP3 and MLKL. Furthermore, the RIP1 inhibitor Nec-1 and the RIP3 inhibitor GSK872 attenuated the killing effect of emodin on U251 cells. In addition, emodin could increase the levels of TNF-α, RIP1, RIP3 and MLKL in vivo. The results demonstrate that emodin could induce necroptosis in glioma possibly through the activation of the TNF-α/RIP1/RIP3 axis. These studies provide novel insight into the induction of necroptosis by emodin and indicate that emodin might be a potential candidate for treating glioma through the necroptosis pathway. |
| doi_str_mv | 10.1007/s10637-019-00764-w |
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Emodin, an anthraquinone compound extracted from rhubarb and other traditional Chinese medicines, has been proven to have a wide range of pharmacological effects, such as anti-inflammatory, antiviral, and antitumor activities. Previous studies have confirmed that emodin has inhibitory effects on various solid tumors, such as osteosarcoma, liver cancer, prostate cancer and glioma. This study aimed to investigate the effects and mechanisms of emodin-induced necroptosis in the glioma cell line U251 by targeting the TNF-α/RIP1/RIP3 signaling pathway. We found that emodin could significantly inhibit U251 cell proliferation, and the viability of U251 cells treated with emodin was reduced in a dose- and time-dependent manner. Flow cytometry assays and Hoechst-PI staining assays showed that emodin induced apoptosis and necroptosis. Real-time PCR and western blot analysis showed that emodin upregulated the levels of TNF-α, RIP1, RIP3 and MLKL. Furthermore, the RIP1 inhibitor Nec-1 and the RIP3 inhibitor GSK872 attenuated the killing effect of emodin on U251 cells. In addition, emodin could increase the levels of TNF-α, RIP1, RIP3 and MLKL in vivo. The results demonstrate that emodin could induce necroptosis in glioma possibly through the activation of the TNF-α/RIP1/RIP3 axis. These studies provide novel insight into the induction of necroptosis by emodin and indicate that emodin might be a potential candidate for treating glioma through the necroptosis pathway.</description><identifier>ISSN: 0167-6997</identifier><identifier>EISSN: 1573-0646</identifier><identifier>DOI: 10.1007/s10637-019-00764-w</identifier><identifier>PMID: 30924024</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Anthraquinone ; Anticancer properties ; Apoptosis ; Biocompatibility ; Biomedical materials ; Bone cancer ; Brain tumors ; Cancer ; Cell Cycle ; Cell Proliferation ; Emodin ; Emodin - pharmacology ; Female ; Flow cytometry ; Glioma ; Glioma - drug therapy ; Glioma - metabolism ; Glioma - pathology ; Glioma cells ; Herbal medicine ; Humans ; Inflammation ; Inhibitors ; Liver ; Liver cancer ; Medicine ; Medicine & Public Health ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Necroptosis ; Necrosis ; Nuclear Pore Complex Proteins - genetics ; Nuclear Pore Complex Proteins - metabolism ; Oncology ; Osteosarcoma ; Pharmacology ; Pharmacology/Toxicology ; Preclinical Studies ; Prostate cancer ; Protein Kinase Inhibitors - pharmacology ; Reactive Oxygen Species - metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases - genetics ; Receptor-Interacting Protein Serine-Threonine Kinases - metabolism ; Rhubarb ; RNA-Binding Proteins - genetics ; RNA-Binding Proteins - metabolism ; Sarcoma ; Signal Transduction ; Solid tumors ; Studies ; Time dependence ; Traditional Chinese medicine ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-α ; Viability ; Xenograft Model Antitumor Assays</subject><ispartof>Investigational new drugs, 2020-02, Vol.38 (1), p.50-59</ispartof><rights>The Author(s) 2019</rights><rights>Investigational New Drugs is a copyright of Springer, (2019). All Rights Reserved. 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-c3dbbb6a62f452c8a1794bd1789b6d83b8e0ae91f9cd7c1dac9d3bcf5413df633</citedby><cites>FETCH-LOGICAL-c474t-c3dbbb6a62f452c8a1794bd1789b6d83b8e0ae91f9cd7c1dac9d3bcf5413df633</cites><orcidid>0000-0002-6558-9405</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10637-019-00764-w$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10637-019-00764-w$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30924024$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Jiabin</creatorcontrib><creatorcontrib>Li, Genhua</creatorcontrib><creatorcontrib>Han, Guangkui</creatorcontrib><creatorcontrib>Feng, Song</creatorcontrib><creatorcontrib>Liu, Yuhan</creatorcontrib><creatorcontrib>Chen, Jun</creatorcontrib><creatorcontrib>Liu, Chen</creatorcontrib><creatorcontrib>Zhao, Lei</creatorcontrib><creatorcontrib>Jin, Feng</creatorcontrib><title>Emodin induced necroptosis in the glioma cell line U251 via the TNF-α/RIP1/RIP3 pathway</title><title>Investigational new drugs</title><addtitle>Invest New Drugs</addtitle><addtitle>Invest New Drugs</addtitle><description>Summary
Emodin, an anthraquinone compound extracted from rhubarb and other traditional Chinese medicines, has been proven to have a wide range of pharmacological effects, such as anti-inflammatory, antiviral, and antitumor activities. Previous studies have confirmed that emodin has inhibitory effects on various solid tumors, such as osteosarcoma, liver cancer, prostate cancer and glioma. This study aimed to investigate the effects and mechanisms of emodin-induced necroptosis in the glioma cell line U251 by targeting the TNF-α/RIP1/RIP3 signaling pathway. We found that emodin could significantly inhibit U251 cell proliferation, and the viability of U251 cells treated with emodin was reduced in a dose- and time-dependent manner. Flow cytometry assays and Hoechst-PI staining assays showed that emodin induced apoptosis and necroptosis. Real-time PCR and western blot analysis showed that emodin upregulated the levels of TNF-α, RIP1, RIP3 and MLKL. Furthermore, the RIP1 inhibitor Nec-1 and the RIP3 inhibitor GSK872 attenuated the killing effect of emodin on U251 cells. In addition, emodin could increase the levels of TNF-α, RIP1, RIP3 and MLKL in vivo. The results demonstrate that emodin could induce necroptosis in glioma possibly through the activation of the TNF-α/RIP1/RIP3 axis. These studies provide novel insight into the induction of necroptosis by emodin and indicate that emodin might be a potential candidate for treating glioma through the necroptosis pathway.</description><subject>Animals</subject><subject>Anthraquinone</subject><subject>Anticancer properties</subject><subject>Apoptosis</subject><subject>Biocompatibility</subject><subject>Biomedical materials</subject><subject>Bone cancer</subject><subject>Brain tumors</subject><subject>Cancer</subject><subject>Cell Cycle</subject><subject>Cell Proliferation</subject><subject>Emodin</subject><subject>Emodin - pharmacology</subject><subject>Female</subject><subject>Flow cytometry</subject><subject>Glioma</subject><subject>Glioma - drug therapy</subject><subject>Glioma - metabolism</subject><subject>Glioma - pathology</subject><subject>Glioma cells</subject><subject>Herbal medicine</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inhibitors</subject><subject>Liver</subject><subject>Liver cancer</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Necroptosis</subject><subject>Necrosis</subject><subject>Nuclear Pore Complex Proteins - genetics</subject><subject>Nuclear Pore Complex Proteins - metabolism</subject><subject>Oncology</subject><subject>Osteosarcoma</subject><subject>Pharmacology</subject><subject>Pharmacology/Toxicology</subject><subject>Preclinical Studies</subject><subject>Prostate cancer</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Receptor-Interacting Protein Serine-Threonine Kinases - genetics</subject><subject>Receptor-Interacting Protein Serine-Threonine Kinases - metabolism</subject><subject>Rhubarb</subject><subject>RNA-Binding Proteins - genetics</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Sarcoma</subject><subject>Signal Transduction</subject><subject>Solid tumors</subject><subject>Studies</subject><subject>Time dependence</subject><subject>Traditional Chinese medicine</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-α</subject><subject>Viability</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0167-6997</issn><issn>1573-0646</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kctu1DAUhi0EokPhBVggS2y6MfUtvmyQUNVCpQoQaiV2lmM7M64Se4iTjvpYvAjPhNMp5bJgY8s-3_nt__wAvCT4DcFYHheCBZMIE43qUXC0ewRWpJEMYcHFY7DCREgktJYH4Fkp1xhjpiV_Cg4Y1pRjylfg6-mQfUwwJj-74GEKbszbKZdY6h2cNgGu-5gHC13oe9jHFOAVbQi8ifauevnxDP34fvzl_DNZFga3dtrs7O1z8KSzfQkv7vdDcHV2ennyAV18en9-8u4COS75hBzzbdsKK2jHG-qUJVLz1hOpdCu8Yq0K2AZNOu28dMRbpz1rXddwwnwnGDsEb_e627kdgnchTaPtzXaMgx1vTbbR_F1JcWPW-cYIrRqsFoGje4Exf5tDmcwQy2LWppDnYihdhiuk1BV9_Q96necxVXuGEq2UwpLyStE9VSdZyhi6h88QbJbgzD44U4Mzd8GZXW169aeNh5ZfSVWA7YFSS2kdxt9v_0f2JyoZpHQ</recordid><startdate>20200201</startdate><enddate>20200201</enddate><creator>Zhou, Jiabin</creator><creator>Li, Genhua</creator><creator>Han, Guangkui</creator><creator>Feng, Song</creator><creator>Liu, Yuhan</creator><creator>Chen, Jun</creator><creator>Liu, Chen</creator><creator>Zhao, Lei</creator><creator>Jin, Feng</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>C6C</scope><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>7QO</scope><scope>7RV</scope><scope>7WY</scope><scope>7WZ</scope><scope>7X7</scope><scope>7XB</scope><scope>87Z</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8FL</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BEZIV</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FRNLG</scope><scope>FYUFA</scope><scope>F~G</scope><scope>GHDGH</scope><scope>K60</scope><scope>K6~</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>L.-</scope><scope>M0C</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQBIZ</scope><scope>PQBZA</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6558-9405</orcidid></search><sort><creationdate>20200201</creationdate><title>Emodin induced necroptosis in the glioma cell line U251 via the TNF-α/RIP1/RIP3 pathway</title><author>Zhou, Jiabin ; Li, Genhua ; Han, Guangkui ; Feng, Song ; Liu, Yuhan ; Chen, Jun ; Liu, Chen ; Zhao, Lei ; Jin, Feng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-c3dbbb6a62f452c8a1794bd1789b6d83b8e0ae91f9cd7c1dac9d3bcf5413df633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Anthraquinone</topic><topic>Anticancer properties</topic><topic>Apoptosis</topic><topic>Biocompatibility</topic><topic>Biomedical materials</topic><topic>Bone cancer</topic><topic>Brain tumors</topic><topic>Cancer</topic><topic>Cell Cycle</topic><topic>Cell Proliferation</topic><topic>Emodin</topic><topic>Emodin - pharmacology</topic><topic>Female</topic><topic>Flow cytometry</topic><topic>Glioma</topic><topic>Glioma - drug therapy</topic><topic>Glioma - metabolism</topic><topic>Glioma - pathology</topic><topic>Glioma cells</topic><topic>Herbal medicine</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inhibitors</topic><topic>Liver</topic><topic>Liver cancer</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Necroptosis</topic><topic>Necrosis</topic><topic>Nuclear Pore Complex Proteins - genetics</topic><topic>Nuclear Pore Complex Proteins - metabolism</topic><topic>Oncology</topic><topic>Osteosarcoma</topic><topic>Pharmacology</topic><topic>Pharmacology/Toxicology</topic><topic>Preclinical Studies</topic><topic>Prostate cancer</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptor-Interacting Protein Serine-Threonine Kinases - genetics</topic><topic>Receptor-Interacting Protein Serine-Threonine Kinases - metabolism</topic><topic>Rhubarb</topic><topic>RNA-Binding Proteins - genetics</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Sarcoma</topic><topic>Signal Transduction</topic><topic>Solid tumors</topic><topic>Studies</topic><topic>Time dependence</topic><topic>Traditional Chinese medicine</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-α</topic><topic>Viability</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Jiabin</creatorcontrib><creatorcontrib>Li, Genhua</creatorcontrib><creatorcontrib>Han, Guangkui</creatorcontrib><creatorcontrib>Feng, Song</creatorcontrib><creatorcontrib>Liu, Yuhan</creatorcontrib><creatorcontrib>Chen, Jun</creatorcontrib><creatorcontrib>Liu, Chen</creatorcontrib><creatorcontrib>Zhao, Lei</creatorcontrib><creatorcontrib>Jin, Feng</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>ABI/INFORM Collection</collection><collection>ABI/INFORM Global (PDF only)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ABI/INFORM Global (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ABI/INFORM Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Business Premium Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Business Premium Collection (Alumni)</collection><collection>Health Research Premium Collection</collection><collection>ABI/INFORM Global (Corporate)</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Business Collection (Alumni Edition)</collection><collection>ProQuest Business Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ABI/INFORM Professional Advanced</collection><collection>ABI/INFORM Global</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Business</collection><collection>ProQuest One Business (Alumni)</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 China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Investigational new drugs</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Jiabin</au><au>Li, Genhua</au><au>Han, Guangkui</au><au>Feng, Song</au><au>Liu, Yuhan</au><au>Chen, Jun</au><au>Liu, Chen</au><au>Zhao, Lei</au><au>Jin, Feng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Emodin induced necroptosis in the glioma cell line U251 via the TNF-α/RIP1/RIP3 pathway</atitle><jtitle>Investigational new drugs</jtitle><stitle>Invest New Drugs</stitle><addtitle>Invest New Drugs</addtitle><date>2020-02-01</date><risdate>2020</risdate><volume>38</volume><issue>1</issue><spage>50</spage><epage>59</epage><pages>50-59</pages><issn>0167-6997</issn><eissn>1573-0646</eissn><abstract>Summary
Emodin, an anthraquinone compound extracted from rhubarb and other traditional Chinese medicines, has been proven to have a wide range of pharmacological effects, such as anti-inflammatory, antiviral, and antitumor activities. Previous studies have confirmed that emodin has inhibitory effects on various solid tumors, such as osteosarcoma, liver cancer, prostate cancer and glioma. This study aimed to investigate the effects and mechanisms of emodin-induced necroptosis in the glioma cell line U251 by targeting the TNF-α/RIP1/RIP3 signaling pathway. We found that emodin could significantly inhibit U251 cell proliferation, and the viability of U251 cells treated with emodin was reduced in a dose- and time-dependent manner. Flow cytometry assays and Hoechst-PI staining assays showed that emodin induced apoptosis and necroptosis. Real-time PCR and western blot analysis showed that emodin upregulated the levels of TNF-α, RIP1, RIP3 and MLKL. Furthermore, the RIP1 inhibitor Nec-1 and the RIP3 inhibitor GSK872 attenuated the killing effect of emodin on U251 cells. In addition, emodin could increase the levels of TNF-α, RIP1, RIP3 and MLKL in vivo. The results demonstrate that emodin could induce necroptosis in glioma possibly through the activation of the TNF-α/RIP1/RIP3 axis. These studies provide novel insight into the induction of necroptosis by emodin and indicate that emodin might be a potential candidate for treating glioma through the necroptosis pathway.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>30924024</pmid><doi>10.1007/s10637-019-00764-w</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-6558-9405</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Anthraquinone Anticancer properties Apoptosis Biocompatibility Biomedical materials Bone cancer Brain tumors Cancer Cell Cycle Cell Proliferation Emodin Emodin - pharmacology Female Flow cytometry Glioma Glioma - drug therapy Glioma - metabolism Glioma - pathology Glioma cells Herbal medicine Humans Inflammation Inhibitors Liver Liver cancer Medicine Medicine & Public Health Mice Mice, Inbred BALB C Mice, Nude Necroptosis Necrosis Nuclear Pore Complex Proteins - genetics Nuclear Pore Complex Proteins - metabolism Oncology Osteosarcoma Pharmacology Pharmacology/Toxicology Preclinical Studies Prostate cancer Protein Kinase Inhibitors - pharmacology Reactive Oxygen Species - metabolism Receptor-Interacting Protein Serine-Threonine Kinases - genetics Receptor-Interacting Protein Serine-Threonine Kinases - metabolism Rhubarb RNA-Binding Proteins - genetics RNA-Binding Proteins - metabolism Sarcoma Signal Transduction Solid tumors Studies Time dependence Traditional Chinese medicine Tumor Cells, Cultured Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-α Viability Xenograft Model Antitumor Assays |
| title | Emodin induced necroptosis in the glioma cell line U251 via the TNF-α/RIP1/RIP3 pathway |
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