The anti-proliferative and anti-inflammatory mechanisms of JAK1 inhibitor SHR0302 versus Ruxolitinib in SET2 cell line and primary cells
To explore the effects and molecular mechanism of the selective JAK1inhibitor SHR0302 and Ruxolitinib on myeloproliterative neoplasms (MPN) cell line SET2 and primary cells in vitro. Cell proliferation was detected by CCK8 kit. Colony forming experiment was conducted to evaluate erythroid burst colo...
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Veröffentlicht in: | Zhōnghuá xuèyèxué zázhì 2019-12, Vol.40 (12), p.1003 |
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container_title | Zhōnghuá xuèyèxué zázhì |
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creator | Yang, A Y Liu, J Q Cai, Y N Fang, M Y Yang, L Chen, M Li, B Xiao, Z J |
description | To explore the effects and molecular mechanism of the selective JAK1inhibitor SHR0302 and Ruxolitinib on myeloproliterative neoplasms (MPN) cell line SET2 and primary cells in vitro.
Cell proliferation was detected by CCK8 kit. Colony forming experiment was conducted to evaluate erythroid burst colony formation unit (BFU-E) of primary cells from MPN patients. Multi-factor kits were used to detect six inflammatory cytokines. Phosphorylated proteins of Jak-Stat signaling pathway were tested by Western blot.
At different time points after treated with SHR0302 and Ruxolitinib, the inhibition of cell proliferation was dose dependent by both drugs ( |
doi_str_mv | 10.3760/cma.j.issn.0253-2727.2019.12.006 |
format | Article |
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Cell proliferation was detected by CCK8 kit. Colony forming experiment was conducted to evaluate erythroid burst colony formation unit (BFU-E) of primary cells from MPN patients. Multi-factor kits were used to detect six inflammatory cytokines. Phosphorylated proteins of Jak-Stat signaling pathway were tested by Western blot.
At different time points after treated with SHR0302 and Ruxolitinib, the inhibition of cell proliferation was dose dependent by both drugs (
<0.01) . The inhibitory rates of 2.5 μmol/L SHR0302 and 0.1 μmol/L Ruxolitinib on SET2 cells for 72 h were comparable, i.e. (59.94±0.60) % and (64.00±0.66) %, respectively, suggesting that the inhibitory effect of SHR0302 was weaker than that of Ruxolitinib. Similarly, both SHR0302 and Ruxolitinib inhibited BFU-E in primary marrow cells from MPN patients in a dose-depen</description><identifier>ISSN: 0253-2727</identifier><identifier>DOI: 10.3760/cma.j.issn.0253-2727.2019.12.006</identifier><identifier>PMID: 32023730</identifier><language>chi</language><publisher>China</publisher><subject>Anti-Inflammatory Agents ; Cell Line ; Cell Proliferation - drug effects ; Histone-Lysine N-Methyltransferase ; Humans ; Janus Kinase 1 ; Nitriles ; Pyrazoles ; Pyrimidines ; Sulfuric Acids</subject><ispartof>Zhōnghuá xuèyèxué zázhì, 2019-12, Vol.40 (12), p.1003</ispartof><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32023730$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, A Y</creatorcontrib><creatorcontrib>Liu, J Q</creatorcontrib><creatorcontrib>Cai, Y N</creatorcontrib><creatorcontrib>Fang, M Y</creatorcontrib><creatorcontrib>Yang, L</creatorcontrib><creatorcontrib>Chen, M</creatorcontrib><creatorcontrib>Li, B</creatorcontrib><creatorcontrib>Xiao, Z J</creatorcontrib><title>The anti-proliferative and anti-inflammatory mechanisms of JAK1 inhibitor SHR0302 versus Ruxolitinib in SET2 cell line and primary cells</title><title>Zhōnghuá xuèyèxué zázhì</title><addtitle>Zhonghua Xue Ye Xue Za Zhi</addtitle><description>To explore the effects and molecular mechanism of the selective JAK1inhibitor SHR0302 and Ruxolitinib on myeloproliterative neoplasms (MPN) cell line SET2 and primary cells in vitro.
Cell proliferation was detected by CCK8 kit. Colony forming experiment was conducted to evaluate erythroid burst colony formation unit (BFU-E) of primary cells from MPN patients. Multi-factor kits were used to detect six inflammatory cytokines. Phosphorylated proteins of Jak-Stat signaling pathway were tested by Western blot.
At different time points after treated with SHR0302 and Ruxolitinib, the inhibition of cell proliferation was dose dependent by both drugs (
<0.01) . The inhibitory rates of 2.5 μmol/L SHR0302 and 0.1 μmol/L Ruxolitinib on SET2 cells for 72 h were comparable, i.e. (59.94±0.60) % and (64.00±0.66) %, respectively, suggesting that the inhibitory effect of SHR0302 was weaker than that of Ruxolitinib. Similarly, both SHR0302 and Ruxolitinib inhibited BFU-E in primary marrow cells from MPN patients in a dose-depen</description><subject>Anti-Inflammatory Agents</subject><subject>Cell Line</subject><subject>Cell Proliferation - drug effects</subject><subject>Histone-Lysine N-Methyltransferase</subject><subject>Humans</subject><subject>Janus Kinase 1</subject><subject>Nitriles</subject><subject>Pyrazoles</subject><subject>Pyrimidines</subject><subject>Sulfuric Acids</subject><issn>0253-2727</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kMtuwjAQRb1oVRDlFyov2SQde7BDlgjRJ1IloOvIcWzhKjY0TlD7B_3sBkG7GunM1dGdIWTCIMVMwr32Kv1IXYwhBS4w4RnPUg4sTxlPAeQVGf7zARnH6EoQDOUMEW7IADlwzBCG5Ge7M1SF1iWHZl87axrVuuMJVWfsgq2V96rdN9_UG71TwUUf6d7Sl_kroy7sXOn6Ld08rQGB06NpYhfpuvvqha0LruxDdLPccqpNXdPahbP_0DiveuuJxltybVUdzfgyR-T9YbldPCWrt8fnxXyVHBiXbcI4mzJZ2cooluc4k9LkJWiutTYWpygkmwplM6kM1zkKYKBYZtGWlVXWII7I5Ozt7_3sTGwL7-KpgQpm38WCo-AgQMygj95dol3pTVVc-hZ_38Nfsz51_Q</recordid><startdate>20191214</startdate><enddate>20191214</enddate><creator>Yang, A Y</creator><creator>Liu, J Q</creator><creator>Cai, Y N</creator><creator>Fang, M Y</creator><creator>Yang, L</creator><creator>Chen, M</creator><creator>Li, B</creator><creator>Xiao, Z J</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20191214</creationdate><title>The anti-proliferative and anti-inflammatory mechanisms of JAK1 inhibitor SHR0302 versus Ruxolitinib in SET2 cell line and primary cells</title><author>Yang, A Y ; Liu, J Q ; Cai, Y N ; Fang, M Y ; Yang, L ; Chen, M ; Li, B ; Xiao, Z J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p126t-121416dfdea1993866e9b0c2cccef34356145af76ae2c935010a17f3fbdfafe33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>chi</language><creationdate>2019</creationdate><topic>Anti-Inflammatory Agents</topic><topic>Cell Line</topic><topic>Cell Proliferation - drug effects</topic><topic>Histone-Lysine N-Methyltransferase</topic><topic>Humans</topic><topic>Janus Kinase 1</topic><topic>Nitriles</topic><topic>Pyrazoles</topic><topic>Pyrimidines</topic><topic>Sulfuric Acids</topic><toplevel>online_resources</toplevel><creatorcontrib>Yang, A Y</creatorcontrib><creatorcontrib>Liu, J Q</creatorcontrib><creatorcontrib>Cai, Y N</creatorcontrib><creatorcontrib>Fang, M Y</creatorcontrib><creatorcontrib>Yang, L</creatorcontrib><creatorcontrib>Chen, M</creatorcontrib><creatorcontrib>Li, B</creatorcontrib><creatorcontrib>Xiao, Z J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Zhōnghuá xuèyèxué zázhì</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, A Y</au><au>Liu, J Q</au><au>Cai, Y N</au><au>Fang, M Y</au><au>Yang, L</au><au>Chen, M</au><au>Li, B</au><au>Xiao, Z J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The anti-proliferative and anti-inflammatory mechanisms of JAK1 inhibitor SHR0302 versus Ruxolitinib in SET2 cell line and primary cells</atitle><jtitle>Zhōnghuá xuèyèxué zázhì</jtitle><addtitle>Zhonghua Xue Ye Xue Za Zhi</addtitle><date>2019-12-14</date><risdate>2019</risdate><volume>40</volume><issue>12</issue><spage>1003</spage><pages>1003-</pages><issn>0253-2727</issn><abstract>To explore the effects and molecular mechanism of the selective JAK1inhibitor SHR0302 and Ruxolitinib on myeloproliterative neoplasms (MPN) cell line SET2 and primary cells in vitro.
Cell proliferation was detected by CCK8 kit. Colony forming experiment was conducted to evaluate erythroid burst colony formation unit (BFU-E) of primary cells from MPN patients. Multi-factor kits were used to detect six inflammatory cytokines. Phosphorylated proteins of Jak-Stat signaling pathway were tested by Western blot.
At different time points after treated with SHR0302 and Ruxolitinib, the inhibition of cell proliferation was dose dependent by both drugs (
<0.01) . The inhibitory rates of 2.5 μmol/L SHR0302 and 0.1 μmol/L Ruxolitinib on SET2 cells for 72 h were comparable, i.e. (59.94±0.60) % and (64.00±0.66) %, respectively, suggesting that the inhibitory effect of SHR0302 was weaker than that of Ruxolitinib. Similarly, both SHR0302 and Ruxolitinib inhibited BFU-E in primary marrow cells from MPN patients in a dose-depen</abstract><cop>China</cop><pmid>32023730</pmid><doi>10.3760/cma.j.issn.0253-2727.2019.12.006</doi></addata></record> |
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source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
subjects | Anti-Inflammatory Agents Cell Line Cell Proliferation - drug effects Histone-Lysine N-Methyltransferase Humans Janus Kinase 1 Nitriles Pyrazoles Pyrimidines Sulfuric Acids |
title | The anti-proliferative and anti-inflammatory mechanisms of JAK1 inhibitor SHR0302 versus Ruxolitinib in SET2 cell line and primary cells |
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