Loading…

Magnolol elicits activation of the extracellular signal-regulated kinase pathway by inducing p27KIP1-mediated G2/M-phase cell cycle arrest in human urinary bladder cancer 5637 cells

Magnolol has been reported to play a role in antitumor activity. However, the relevant pathway integrating cell cycle regulation and signaling pathways involved in growth inhibition in cancer cells remains to be identified. In the present study, magnolol treatment of these cells resulted in signific...

Full description

Saved in:
Bibliographic Details
Published in:Biochemical pharmacology 2008-06, Vol.75 (12), p.2289-2300
Main Authors: Lee, Se-Jung, Cho, Young-Hwa, Park, Keerang, Kim, Eun-Jung, Jung, Kyung-Hwan, Park, Sung-Soo, Kim, Wun-Jae, Moon, Sung-Kwon
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c478t-4cdc6c5756c5e9d4c200e0c3bb0a57a9c79ba51304b13604ac98d9109919a8bb3
cites cdi_FETCH-LOGICAL-c478t-4cdc6c5756c5e9d4c200e0c3bb0a57a9c79ba51304b13604ac98d9109919a8bb3
container_end_page 2300
container_issue 12
container_start_page 2289
container_title Biochemical pharmacology
container_volume 75
creator Lee, Se-Jung
Cho, Young-Hwa
Park, Keerang
Kim, Eun-Jung
Jung, Kyung-Hwan
Park, Sung-Soo
Kim, Wun-Jae
Moon, Sung-Kwon
description Magnolol has been reported to play a role in antitumor activity. However, the relevant pathway integrating cell cycle regulation and signaling pathways involved in growth inhibition in cancer cells remains to be identified. In the present study, magnolol treatment of these cells resulted in significant dose-dependent growth inhibition together with apoptosis, G1- and G2/M-phase cell cycle arrest at a 60 μM (IC 50) dose in 5637 bladder cancer cells. In addition, magnolol treatment strongly induced p27KIP1 expression, and down-regulated expression of cyclin-dependent kinases (CDKs) and cyclins. Moreover, treatment with magnolol-induced phosphorylation of ERK, p38 MAP kinase, and JNK. Among the pathway inhibitors examined, only PD98059, an ERK-specific inhibitor, blocked magnolol-dependent p27KIP1 expression. Blockade of ERK function consistently reversed magnolol-mediated inhibition of cell proliferation and decreased G2/M cell cycle proteins, but not G1 cell cycle proteins. Furthermore, magnolol treatment increased both Ras and Raf activation. Transfection of cells with dominant negative Ras (RasN17) and Raf (RafS621A) mutant genes suppressed magnolol-induced ERK activity and p27KIP1 expression. Finally, the magnolol-induced reduction in cell proliferation and G2/M cell cycle proteins was also abolished in the presence of RasN17 and RafS621A mutant genes. These data demonstrate that the Ras/Raf/ERK pathway participates in p27KIP1 induction, leading to a decrease in the levels of cyclin B1/Cdc2 complexes and magnolol-dependent inhibition of cell growth. Overall, these novel findings concerning the molecular mechanisms of magnolol in 5637 bladder cancer cells provide a theoretical basis for therapeutic treatment of malignancies.
doi_str_mv 10.1016/j.bcp.2008.03.022
format article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71625464</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0006295208002050</els_id><sourcerecordid>71625464</sourcerecordid><originalsourceid>FETCH-LOGICAL-c478t-4cdc6c5756c5e9d4c200e0c3bb0a57a9c79ba51304b13604ac98d9109919a8bb3</originalsourceid><addsrcrecordid>eNqFkc9u1DAQxi0EokvhAbggX-CW1M4fOxYnVJVS0QoOcLYmY--uF28SbKewD8b74XRXcIOLxyP95tPM9xHykrOSMy4udmWPU1kx1pWsLllVPSIr3sm6qJToHpMVY0zkf1udkWcx7pa2E_wpOeNdI7pWdivy6w42w-hHT6136FKkgMndQ3LjQMc1TVtL7c8UAK33s4dAo9sM4ItgN7lN1tBvboBo6QRp-wMOtD9QN5gZ3bChUyU_3nzmxd4a98BeVxd3xbRd-EWQ4gG9pRCCjSmP0e28h4HOIUuGLOXBGBsowoC5tKKWD2PxOXmyBh_ti1M9J1_fX325_FDcfrq-uXx3W2Aju1Q0aFBgK9v8WGUazFZZhnXfM2glKJSqh5bXrOl5LVgDqDqjOFOKK-j6vj4nb466Uxi_z3lHvXdx2QAGO85RSy6qthHNf0GupMrBLCA_ghjGGINd6ym4fT5Wc6aXUPVO51D1Eqpmtc6h5plXJ_G5z07-nTilmIHXJwAigl-H7JeLf7iKNfmmeuHeHjmbPbt3NuiIzmZvjQsWkzaj-8cavwFWTcEL</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>19798734</pqid></control><display><type>article</type><title>Magnolol elicits activation of the extracellular signal-regulated kinase pathway by inducing p27KIP1-mediated G2/M-phase cell cycle arrest in human urinary bladder cancer 5637 cells</title><source>ScienceDirect Journals</source><creator>Lee, Se-Jung ; Cho, Young-Hwa ; Park, Keerang ; Kim, Eun-Jung ; Jung, Kyung-Hwan ; Park, Sung-Soo ; Kim, Wun-Jae ; Moon, Sung-Kwon</creator><creatorcontrib>Lee, Se-Jung ; Cho, Young-Hwa ; Park, Keerang ; Kim, Eun-Jung ; Jung, Kyung-Hwan ; Park, Sung-Soo ; Kim, Wun-Jae ; Moon, Sung-Kwon</creatorcontrib><description>Magnolol has been reported to play a role in antitumor activity. However, the relevant pathway integrating cell cycle regulation and signaling pathways involved in growth inhibition in cancer cells remains to be identified. In the present study, magnolol treatment of these cells resulted in significant dose-dependent growth inhibition together with apoptosis, G1- and G2/M-phase cell cycle arrest at a 60 μM (IC 50) dose in 5637 bladder cancer cells. In addition, magnolol treatment strongly induced p27KIP1 expression, and down-regulated expression of cyclin-dependent kinases (CDKs) and cyclins. Moreover, treatment with magnolol-induced phosphorylation of ERK, p38 MAP kinase, and JNK. Among the pathway inhibitors examined, only PD98059, an ERK-specific inhibitor, blocked magnolol-dependent p27KIP1 expression. Blockade of ERK function consistently reversed magnolol-mediated inhibition of cell proliferation and decreased G2/M cell cycle proteins, but not G1 cell cycle proteins. Furthermore, magnolol treatment increased both Ras and Raf activation. Transfection of cells with dominant negative Ras (RasN17) and Raf (RafS621A) mutant genes suppressed magnolol-induced ERK activity and p27KIP1 expression. Finally, the magnolol-induced reduction in cell proliferation and G2/M cell cycle proteins was also abolished in the presence of RasN17 and RafS621A mutant genes. These data demonstrate that the Ras/Raf/ERK pathway participates in p27KIP1 induction, leading to a decrease in the levels of cyclin B1/Cdc2 complexes and magnolol-dependent inhibition of cell growth. Overall, these novel findings concerning the molecular mechanisms of magnolol in 5637 bladder cancer cells provide a theoretical basis for therapeutic treatment of malignancies.</description><identifier>ISSN: 0006-2952</identifier><identifier>EISSN: 1873-2968</identifier><identifier>DOI: 10.1016/j.bcp.2008.03.022</identifier><identifier>PMID: 18468578</identifier><identifier>CODEN: BCPCA6</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Antineoplastic Agents, Phytogenic - pharmacology ; Apoptosis - drug effects ; Biological and medical sciences ; Biphenyl Compounds - pharmacology ; Bladder cancer 5637 cells ; Cell Cycle - drug effects ; Cell Division - drug effects ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cyclin-Dependent Kinase Inhibitor p27 - biosynthesis ; Dose-Response Relationship, Drug ; Enzyme Inhibitors - pharmacology ; Extracellular Signal-Regulated MAP Kinases - metabolism ; G2 Phase - drug effects ; G2/M-phase cell cycle arrest ; Humans ; Lignans - pharmacology ; Magnolol ; Medical sciences ; Nephrology. Urinary tract diseases ; p27KIP1 ; Pharmacology. Drug treatments ; Phosphorylation ; Signal Transduction - drug effects ; Tumors of the urinary system ; Urinary Bladder Neoplasms - enzymology ; Urinary Bladder Neoplasms - pathology ; Urinary system involvement in other diseases. Miscellaneous ; Urinary tract. Prostate gland</subject><ispartof>Biochemical pharmacology, 2008-06, Vol.75 (12), p.2289-2300</ispartof><rights>2008 Elsevier Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-4cdc6c5756c5e9d4c200e0c3bb0a57a9c79ba51304b13604ac98d9109919a8bb3</citedby><cites>FETCH-LOGICAL-c478t-4cdc6c5756c5e9d4c200e0c3bb0a57a9c79ba51304b13604ac98d9109919a8bb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=20410938$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18468578$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Se-Jung</creatorcontrib><creatorcontrib>Cho, Young-Hwa</creatorcontrib><creatorcontrib>Park, Keerang</creatorcontrib><creatorcontrib>Kim, Eun-Jung</creatorcontrib><creatorcontrib>Jung, Kyung-Hwan</creatorcontrib><creatorcontrib>Park, Sung-Soo</creatorcontrib><creatorcontrib>Kim, Wun-Jae</creatorcontrib><creatorcontrib>Moon, Sung-Kwon</creatorcontrib><title>Magnolol elicits activation of the extracellular signal-regulated kinase pathway by inducing p27KIP1-mediated G2/M-phase cell cycle arrest in human urinary bladder cancer 5637 cells</title><title>Biochemical pharmacology</title><addtitle>Biochem Pharmacol</addtitle><description>Magnolol has been reported to play a role in antitumor activity. However, the relevant pathway integrating cell cycle regulation and signaling pathways involved in growth inhibition in cancer cells remains to be identified. In the present study, magnolol treatment of these cells resulted in significant dose-dependent growth inhibition together with apoptosis, G1- and G2/M-phase cell cycle arrest at a 60 μM (IC 50) dose in 5637 bladder cancer cells. In addition, magnolol treatment strongly induced p27KIP1 expression, and down-regulated expression of cyclin-dependent kinases (CDKs) and cyclins. Moreover, treatment with magnolol-induced phosphorylation of ERK, p38 MAP kinase, and JNK. Among the pathway inhibitors examined, only PD98059, an ERK-specific inhibitor, blocked magnolol-dependent p27KIP1 expression. Blockade of ERK function consistently reversed magnolol-mediated inhibition of cell proliferation and decreased G2/M cell cycle proteins, but not G1 cell cycle proteins. Furthermore, magnolol treatment increased both Ras and Raf activation. Transfection of cells with dominant negative Ras (RasN17) and Raf (RafS621A) mutant genes suppressed magnolol-induced ERK activity and p27KIP1 expression. Finally, the magnolol-induced reduction in cell proliferation and G2/M cell cycle proteins was also abolished in the presence of RasN17 and RafS621A mutant genes. These data demonstrate that the Ras/Raf/ERK pathway participates in p27KIP1 induction, leading to a decrease in the levels of cyclin B1/Cdc2 complexes and magnolol-dependent inhibition of cell growth. Overall, these novel findings concerning the molecular mechanisms of magnolol in 5637 bladder cancer cells provide a theoretical basis for therapeutic treatment of malignancies.</description><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Biphenyl Compounds - pharmacology</subject><subject>Bladder cancer 5637 cells</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Division - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cyclin-Dependent Kinase Inhibitor p27 - biosynthesis</subject><subject>Dose-Response Relationship, Drug</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>G2 Phase - drug effects</subject><subject>G2/M-phase cell cycle arrest</subject><subject>Humans</subject><subject>Lignans - pharmacology</subject><subject>Magnolol</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>p27KIP1</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphorylation</subject><subject>Signal Transduction - drug effects</subject><subject>Tumors of the urinary system</subject><subject>Urinary Bladder Neoplasms - enzymology</subject><subject>Urinary Bladder Neoplasms - pathology</subject><subject>Urinary system involvement in other diseases. Miscellaneous</subject><subject>Urinary tract. Prostate gland</subject><issn>0006-2952</issn><issn>1873-2968</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNqFkc9u1DAQxi0EokvhAbggX-CW1M4fOxYnVJVS0QoOcLYmY--uF28SbKewD8b74XRXcIOLxyP95tPM9xHykrOSMy4udmWPU1kx1pWsLllVPSIr3sm6qJToHpMVY0zkf1udkWcx7pa2E_wpOeNdI7pWdivy6w42w-hHT6136FKkgMndQ3LjQMc1TVtL7c8UAK33s4dAo9sM4ItgN7lN1tBvboBo6QRp-wMOtD9QN5gZ3bChUyU_3nzmxd4a98BeVxd3xbRd-EWQ4gG9pRCCjSmP0e28h4HOIUuGLOXBGBsowoC5tKKWD2PxOXmyBh_ti1M9J1_fX325_FDcfrq-uXx3W2Aju1Q0aFBgK9v8WGUazFZZhnXfM2glKJSqh5bXrOl5LVgDqDqjOFOKK-j6vj4nb466Uxi_z3lHvXdx2QAGO85RSy6qthHNf0GupMrBLCA_ghjGGINd6ym4fT5Wc6aXUPVO51D1Eqpmtc6h5plXJ_G5z07-nTilmIHXJwAigl-H7JeLf7iKNfmmeuHeHjmbPbt3NuiIzmZvjQsWkzaj-8cavwFWTcEL</recordid><startdate>20080615</startdate><enddate>20080615</enddate><creator>Lee, Se-Jung</creator><creator>Cho, Young-Hwa</creator><creator>Park, Keerang</creator><creator>Kim, Eun-Jung</creator><creator>Jung, Kyung-Hwan</creator><creator>Park, Sung-Soo</creator><creator>Kim, Wun-Jae</creator><creator>Moon, Sung-Kwon</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>IQODW</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20080615</creationdate><title>Magnolol elicits activation of the extracellular signal-regulated kinase pathway by inducing p27KIP1-mediated G2/M-phase cell cycle arrest in human urinary bladder cancer 5637 cells</title><author>Lee, Se-Jung ; Cho, Young-Hwa ; Park, Keerang ; Kim, Eun-Jung ; Jung, Kyung-Hwan ; Park, Sung-Soo ; Kim, Wun-Jae ; Moon, Sung-Kwon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-4cdc6c5756c5e9d4c200e0c3bb0a57a9c79ba51304b13604ac98d9109919a8bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Biphenyl Compounds - pharmacology</topic><topic>Bladder cancer 5637 cells</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Division - drug effects</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cyclin-Dependent Kinase Inhibitor p27 - biosynthesis</topic><topic>Dose-Response Relationship, Drug</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>G2 Phase - drug effects</topic><topic>G2/M-phase cell cycle arrest</topic><topic>Humans</topic><topic>Lignans - pharmacology</topic><topic>Magnolol</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>p27KIP1</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphorylation</topic><topic>Signal Transduction - drug effects</topic><topic>Tumors of the urinary system</topic><topic>Urinary Bladder Neoplasms - enzymology</topic><topic>Urinary Bladder Neoplasms - pathology</topic><topic>Urinary system involvement in other diseases. Miscellaneous</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Se-Jung</creatorcontrib><creatorcontrib>Cho, Young-Hwa</creatorcontrib><creatorcontrib>Park, Keerang</creatorcontrib><creatorcontrib>Kim, Eun-Jung</creatorcontrib><creatorcontrib>Jung, Kyung-Hwan</creatorcontrib><creatorcontrib>Park, Sung-Soo</creatorcontrib><creatorcontrib>Kim, Wun-Jae</creatorcontrib><creatorcontrib>Moon, Sung-Kwon</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Se-Jung</au><au>Cho, Young-Hwa</au><au>Park, Keerang</au><au>Kim, Eun-Jung</au><au>Jung, Kyung-Hwan</au><au>Park, Sung-Soo</au><au>Kim, Wun-Jae</au><au>Moon, Sung-Kwon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Magnolol elicits activation of the extracellular signal-regulated kinase pathway by inducing p27KIP1-mediated G2/M-phase cell cycle arrest in human urinary bladder cancer 5637 cells</atitle><jtitle>Biochemical pharmacology</jtitle><addtitle>Biochem Pharmacol</addtitle><date>2008-06-15</date><risdate>2008</risdate><volume>75</volume><issue>12</issue><spage>2289</spage><epage>2300</epage><pages>2289-2300</pages><issn>0006-2952</issn><eissn>1873-2968</eissn><coden>BCPCA6</coden><abstract>Magnolol has been reported to play a role in antitumor activity. However, the relevant pathway integrating cell cycle regulation and signaling pathways involved in growth inhibition in cancer cells remains to be identified. In the present study, magnolol treatment of these cells resulted in significant dose-dependent growth inhibition together with apoptosis, G1- and G2/M-phase cell cycle arrest at a 60 μM (IC 50) dose in 5637 bladder cancer cells. In addition, magnolol treatment strongly induced p27KIP1 expression, and down-regulated expression of cyclin-dependent kinases (CDKs) and cyclins. Moreover, treatment with magnolol-induced phosphorylation of ERK, p38 MAP kinase, and JNK. Among the pathway inhibitors examined, only PD98059, an ERK-specific inhibitor, blocked magnolol-dependent p27KIP1 expression. Blockade of ERK function consistently reversed magnolol-mediated inhibition of cell proliferation and decreased G2/M cell cycle proteins, but not G1 cell cycle proteins. Furthermore, magnolol treatment increased both Ras and Raf activation. Transfection of cells with dominant negative Ras (RasN17) and Raf (RafS621A) mutant genes suppressed magnolol-induced ERK activity and p27KIP1 expression. Finally, the magnolol-induced reduction in cell proliferation and G2/M cell cycle proteins was also abolished in the presence of RasN17 and RafS621A mutant genes. These data demonstrate that the Ras/Raf/ERK pathway participates in p27KIP1 induction, leading to a decrease in the levels of cyclin B1/Cdc2 complexes and magnolol-dependent inhibition of cell growth. Overall, these novel findings concerning the molecular mechanisms of magnolol in 5637 bladder cancer cells provide a theoretical basis for therapeutic treatment of malignancies.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>18468578</pmid><doi>10.1016/j.bcp.2008.03.022</doi><tpages>12</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0006-2952
ispartof Biochemical pharmacology, 2008-06, Vol.75 (12), p.2289-2300
issn 0006-2952
1873-2968
language eng
recordid cdi_proquest_miscellaneous_71625464
source ScienceDirect Journals
subjects Antineoplastic Agents, Phytogenic - pharmacology
Apoptosis - drug effects
Biological and medical sciences
Biphenyl Compounds - pharmacology
Bladder cancer 5637 cells
Cell Cycle - drug effects
Cell Division - drug effects
Cell Line, Tumor
Cell Proliferation - drug effects
Cell Survival - drug effects
Cyclin-Dependent Kinase Inhibitor p27 - biosynthesis
Dose-Response Relationship, Drug
Enzyme Inhibitors - pharmacology
Extracellular Signal-Regulated MAP Kinases - metabolism
G2 Phase - drug effects
G2/M-phase cell cycle arrest
Humans
Lignans - pharmacology
Magnolol
Medical sciences
Nephrology. Urinary tract diseases
p27KIP1
Pharmacology. Drug treatments
Phosphorylation
Signal Transduction - drug effects
Tumors of the urinary system
Urinary Bladder Neoplasms - enzymology
Urinary Bladder Neoplasms - pathology
Urinary system involvement in other diseases. Miscellaneous
Urinary tract. Prostate gland
title Magnolol elicits activation of the extracellular signal-regulated kinase pathway by inducing p27KIP1-mediated G2/M-phase cell cycle arrest in human urinary bladder cancer 5637 cells
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T17%3A40%3A48IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Magnolol%20elicits%20activation%20of%20the%20extracellular%20signal-regulated%20kinase%20pathway%20by%20inducing%20p27KIP1-mediated%20G2/M-phase%20cell%20cycle%20arrest%20in%20human%20urinary%20bladder%20cancer%205637%20cells&rft.jtitle=Biochemical%20pharmacology&rft.au=Lee,%20Se-Jung&rft.date=2008-06-15&rft.volume=75&rft.issue=12&rft.spage=2289&rft.epage=2300&rft.pages=2289-2300&rft.issn=0006-2952&rft.eissn=1873-2968&rft.coden=BCPCA6&rft_id=info:doi/10.1016/j.bcp.2008.03.022&rft_dat=%3Cproquest_cross%3E71625464%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c478t-4cdc6c5756c5e9d4c200e0c3bb0a57a9c79ba51304b13604ac98d9109919a8bb3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=19798734&rft_id=info:pmid/18468578&rfr_iscdi=true