Glycyrrhetinic acid induces G1-phase cell cycle arrest in human non-small cell lung cancer cells through endoplasmic reticulum stress pathway
Glycyrrhetinic acid (GA) is a natural compound extracted from liquorice, which is often used in traditional Chinese medicine. The purpose of the present study was to investigate the antitumor effect of GA in human non-small cell lung cancer (NSCLC), and its underlying mechanisms in vitro. We have sh...
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| Veröffentlicht in: | International journal of oncology 2015-03, Vol.46 (3), p.981-988 |
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| creator | ZHU, JIE CHEN, MEIJUAN CHEN, NING MA, AIZHEN ZHU, CHUNYAN ZHAO, RUOLIN JIANG, MIAO ZHOU, JING YE, LIHONG FU, HAIAN ZHANG, XU |
| description | Glycyrrhetinic acid (GA) is a natural compound extracted from liquorice, which is often used in traditional Chinese medicine. The purpose of the present study was to investigate the antitumor effect of GA in human non-small cell lung cancer (NSCLC), and its underlying mechanisms in vitro. We have shown that GA suppressed the proliferation of A549 and NCI-H460 cells. Flow cytometric analysis showed that GA arrested cell cycle in G0/G1 phase without inducing apoptosis. Western blot analysis indicated that GA mediated G1-phase cell cycle arrest by upregulation of cyclin-dependent kinase inhibitors (CKIs) (p18, p16, p27 and p21) and inhibition of cyclins (cyclin-D1, -D3 and -E) and cyclin-dependent kinases (CDKs) (CDK4, 6 and 2). GA also maintained pRb phosphorylation status, and inhibited E2F transcription factor 1 (E2F-1) in both cell lines. GA upregulated the unfolded proteins, Bip, PERK and ERP72. Accumulation of unfolded proteins in the endoplasmic reticulum (ER) triggered the unfolded protein response (UPR), which could be the mechanism by which GA inhibited cell proliferation in NSCLC cells. GA then coordinated the induction of ER chaperones, which decreased protein synthesis and induced cell cycle arrest in the G1 phase. This study provides experimental evidence to support the development of GA as a chemotherapeutic agent for NSCLC. |
| doi_str_mv | 10.3892/ijo.2015.2819 |
| format | Article |
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The purpose of the present study was to investigate the antitumor effect of GA in human non-small cell lung cancer (NSCLC), and its underlying mechanisms in vitro. We have shown that GA suppressed the proliferation of A549 and NCI-H460 cells. Flow cytometric analysis showed that GA arrested cell cycle in G0/G1 phase without inducing apoptosis. Western blot analysis indicated that GA mediated G1-phase cell cycle arrest by upregulation of cyclin-dependent kinase inhibitors (CKIs) (p18, p16, p27 and p21) and inhibition of cyclins (cyclin-D1, -D3 and -E) and cyclin-dependent kinases (CDKs) (CDK4, 6 and 2). GA also maintained pRb phosphorylation status, and inhibited E2F transcription factor 1 (E2F-1) in both cell lines. GA upregulated the unfolded proteins, Bip, PERK and ERP72. Accumulation of unfolded proteins in the endoplasmic reticulum (ER) triggered the unfolded protein response (UPR), which could be the mechanism by which GA inhibited cell proliferation in NSCLC cells. GA then coordinated the induction of ER chaperones, which decreased protein synthesis and induced cell cycle arrest in the G1 phase. This study provides experimental evidence to support the development of GA as a chemotherapeutic agent for NSCLC.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2015.2819</identifier><identifier>PMID: 25573651</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Analysis ; Antineoplastic Agents - pharmacology ; Apoptosis ; Cancer therapies ; Carcinoma, Non-Small-Cell Lung - drug therapy ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Care and treatment ; Cell cycle ; cell cycle arrest ; Cell Line, Tumor - drug effects ; Cell Proliferation - drug effects ; Cyclins - metabolism ; Drugs, Chinese Herbal - pharmacology ; Endoplasmic reticulum ; Endoplasmic Reticulum Stress - drug effects ; ER stress ; G1 Phase Cell Cycle Checkpoints - drug effects ; Gene expression ; glycyrrhetinic acid ; Glycyrrhetinic Acid - pharmacology ; Health aspects ; Heat-Shock Proteins - metabolism ; Humans ; Immunoglobulins ; Kinases ; Lung cancer ; Lung cancer, Non-small cell ; Lung Neoplasms - drug therapy ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Medicine, Chinese ; Membrane Glycoproteins - metabolism ; NSCLC ; Phosphorylation - drug effects ; Protein synthesis ; Proteins ; Retinoblastoma Protein - metabolism ; Transcription factors ; Variance analysis</subject><ispartof>International journal of oncology, 2015-03, Vol.46 (3), p.981-988</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><rights>Copyright © 2015, Spandidos Publications 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c545t-4797c42c0c34b62f169aa0685101914c3822bc0ff337146317f88ddc5737241b3</citedby><cites>FETCH-LOGICAL-c545t-4797c42c0c34b62f169aa0685101914c3822bc0ff337146317f88ddc5737241b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25573651$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ZHU, JIE</creatorcontrib><creatorcontrib>CHEN, MEIJUAN</creatorcontrib><creatorcontrib>CHEN, NING</creatorcontrib><creatorcontrib>MA, AIZHEN</creatorcontrib><creatorcontrib>ZHU, CHUNYAN</creatorcontrib><creatorcontrib>ZHAO, RUOLIN</creatorcontrib><creatorcontrib>JIANG, MIAO</creatorcontrib><creatorcontrib>ZHOU, JING</creatorcontrib><creatorcontrib>YE, LIHONG</creatorcontrib><creatorcontrib>FU, HAIAN</creatorcontrib><creatorcontrib>ZHANG, XU</creatorcontrib><title>Glycyrrhetinic acid induces G1-phase cell cycle arrest in human non-small cell lung cancer cells through endoplasmic reticulum stress pathway</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>Glycyrrhetinic acid (GA) is a natural compound extracted from liquorice, which is often used in traditional Chinese medicine. The purpose of the present study was to investigate the antitumor effect of GA in human non-small cell lung cancer (NSCLC), and its underlying mechanisms in vitro. We have shown that GA suppressed the proliferation of A549 and NCI-H460 cells. Flow cytometric analysis showed that GA arrested cell cycle in G0/G1 phase without inducing apoptosis. Western blot analysis indicated that GA mediated G1-phase cell cycle arrest by upregulation of cyclin-dependent kinase inhibitors (CKIs) (p18, p16, p27 and p21) and inhibition of cyclins (cyclin-D1, -D3 and -E) and cyclin-dependent kinases (CDKs) (CDK4, 6 and 2). GA also maintained pRb phosphorylation status, and inhibited E2F transcription factor 1 (E2F-1) in both cell lines. GA upregulated the unfolded proteins, Bip, PERK and ERP72. Accumulation of unfolded proteins in the endoplasmic reticulum (ER) triggered the unfolded protein response (UPR), which could be the mechanism by which GA inhibited cell proliferation in NSCLC cells. GA then coordinated the induction of ER chaperones, which decreased protein synthesis and induced cell cycle arrest in the G1 phase. This study provides experimental evidence to support the development of GA as a chemotherapeutic agent for NSCLC.</description><subject>Analysis</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Cancer therapies</subject><subject>Carcinoma, Non-Small-Cell Lung - drug therapy</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>cell cycle arrest</subject><subject>Cell Line, Tumor - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cyclins - metabolism</subject><subject>Drugs, Chinese Herbal - pharmacology</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum Stress - drug effects</subject><subject>ER stress</subject><subject>G1 Phase Cell Cycle Checkpoints - drug effects</subject><subject>Gene expression</subject><subject>glycyrrhetinic acid</subject><subject>Glycyrrhetinic Acid - pharmacology</subject><subject>Health aspects</subject><subject>Heat-Shock Proteins - metabolism</subject><subject>Humans</subject><subject>Immunoglobulins</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Lung cancer, Non-small cell</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Medicine, Chinese</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>NSCLC</subject><subject>Phosphorylation - drug effects</subject><subject>Protein synthesis</subject><subject>Proteins</subject><subject>Retinoblastoma Protein - metabolism</subject><subject>Transcription factors</subject><subject>Variance analysis</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkk2LFDEQhhtR3HX16FUCgnvKmK_-ugjL4o7Cghc9h0x1ejpDOmmTjtI_wv9s2lnHHZAcKlQ9eStVvEXxmpINb1r23hz8hhFablhD2yfFJa1biplg_Gm-E9riSvD2ongR44EQVpaEPi8ucqx5VdLL4tfWLrCEMOjZOANIgemQcV0CHdGW4mlQUSPQ1iJYwGqkQtBxzgga0qgcct7hOKq1vkI2uT0C5UCHP4mI5iH4tB-Qdp2frIpj7hJyN0g2jSjOWS6iSc3DT7W8LJ71ykb96iFeFd_uPn69_YTvv2w_397cYyhFOWNRtzUIBgS42FWsp1WrFKmach2YCuANYzsgfc95TUXFad03TddBHrpmgu74VfHhqDul3ag70G4OysopmFGFRXpl5HnFmUHu_Q8pOBNlQ7LA2weB4L-nvBB58Cm4_GdJW844J6Jp_1F7ZbU0rvdZDEYTQd4IXpMMNSxTm_9Q-XQ678o73ZucP3vw7tGDQSs7D9HbNBvv4jmIjyAEH2PQ_WlCSuTqHpndI1f3yNU9mX_zeC0n-q9dMnB9BOKkXGc6H09MVsKiwoRj0jaU_wbR9M1Q</recordid><startdate>20150301</startdate><enddate>20150301</enddate><creator>ZHU, JIE</creator><creator>CHEN, MEIJUAN</creator><creator>CHEN, NING</creator><creator>MA, AIZHEN</creator><creator>ZHU, CHUNYAN</creator><creator>ZHAO, RUOLIN</creator><creator>JIANG, MIAO</creator><creator>ZHOU, JING</creator><creator>YE, LIHONG</creator><creator>FU, HAIAN</creator><creator>ZHANG, XU</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20150301</creationdate><title>Glycyrrhetinic acid induces G1-phase cell cycle arrest in human non-small cell lung cancer cells through endoplasmic reticulum stress pathway</title><author>ZHU, JIE ; CHEN, MEIJUAN ; CHEN, NING ; MA, AIZHEN ; ZHU, CHUNYAN ; ZHAO, RUOLIN ; JIANG, MIAO ; ZHOU, JING ; YE, LIHONG ; FU, HAIAN ; ZHANG, XU</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c545t-4797c42c0c34b62f169aa0685101914c3822bc0ff337146317f88ddc5737241b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Analysis</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Cancer therapies</topic><topic>Carcinoma, Non-Small-Cell Lung - drug therapy</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>cell cycle arrest</topic><topic>Cell Line, Tumor - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cyclins - metabolism</topic><topic>Drugs, Chinese Herbal - pharmacology</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>ER stress</topic><topic>G1 Phase Cell Cycle Checkpoints - drug effects</topic><topic>Gene expression</topic><topic>glycyrrhetinic acid</topic><topic>Glycyrrhetinic Acid - pharmacology</topic><topic>Health aspects</topic><topic>Heat-Shock Proteins - metabolism</topic><topic>Humans</topic><topic>Immunoglobulins</topic><topic>Kinases</topic><topic>Lung cancer</topic><topic>Lung cancer, Non-small cell</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Medicine, Chinese</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>NSCLC</topic><topic>Phosphorylation - drug effects</topic><topic>Protein synthesis</topic><topic>Proteins</topic><topic>Retinoblastoma Protein - metabolism</topic><topic>Transcription factors</topic><topic>Variance analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ZHU, JIE</creatorcontrib><creatorcontrib>CHEN, MEIJUAN</creatorcontrib><creatorcontrib>CHEN, NING</creatorcontrib><creatorcontrib>MA, AIZHEN</creatorcontrib><creatorcontrib>ZHU, CHUNYAN</creatorcontrib><creatorcontrib>ZHAO, RUOLIN</creatorcontrib><creatorcontrib>JIANG, MIAO</creatorcontrib><creatorcontrib>ZHOU, JING</creatorcontrib><creatorcontrib>YE, LIHONG</creatorcontrib><creatorcontrib>FU, HAIAN</creatorcontrib><creatorcontrib>ZHANG, XU</creatorcontrib><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>Proquest Nursing & Allied Health Source</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>PubMed Central (Full Participant titles)</collection><jtitle>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ZHU, JIE</au><au>CHEN, MEIJUAN</au><au>CHEN, NING</au><au>MA, AIZHEN</au><au>ZHU, CHUNYAN</au><au>ZHAO, RUOLIN</au><au>JIANG, MIAO</au><au>ZHOU, JING</au><au>YE, LIHONG</au><au>FU, HAIAN</au><au>ZHANG, XU</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glycyrrhetinic acid induces G1-phase cell cycle arrest in human non-small cell lung cancer cells through endoplasmic reticulum stress pathway</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2015-03-01</date><risdate>2015</risdate><volume>46</volume><issue>3</issue><spage>981</spage><epage>988</epage><pages>981-988</pages><issn>1019-6439</issn><eissn>1791-2423</eissn><abstract>Glycyrrhetinic acid (GA) is a natural compound extracted from liquorice, which is often used in traditional Chinese medicine. The purpose of the present study was to investigate the antitumor effect of GA in human non-small cell lung cancer (NSCLC), and its underlying mechanisms in vitro. We have shown that GA suppressed the proliferation of A549 and NCI-H460 cells. Flow cytometric analysis showed that GA arrested cell cycle in G0/G1 phase without inducing apoptosis. Western blot analysis indicated that GA mediated G1-phase cell cycle arrest by upregulation of cyclin-dependent kinase inhibitors (CKIs) (p18, p16, p27 and p21) and inhibition of cyclins (cyclin-D1, -D3 and -E) and cyclin-dependent kinases (CDKs) (CDK4, 6 and 2). GA also maintained pRb phosphorylation status, and inhibited E2F transcription factor 1 (E2F-1) in both cell lines. GA upregulated the unfolded proteins, Bip, PERK and ERP72. Accumulation of unfolded proteins in the endoplasmic reticulum (ER) triggered the unfolded protein response (UPR), which could be the mechanism by which GA inhibited cell proliferation in NSCLC cells. GA then coordinated the induction of ER chaperones, which decreased protein synthesis and induced cell cycle arrest in the G1 phase. This study provides experimental evidence to support the development of GA as a chemotherapeutic agent for NSCLC.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25573651</pmid><doi>10.3892/ijo.2015.2819</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of oncology, 2015-03, Vol.46 (3), p.981-988 |
| issn | 1019-6439 1791-2423 |
| language | eng |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Analysis Antineoplastic Agents - pharmacology Apoptosis Cancer therapies Carcinoma, Non-Small-Cell Lung - drug therapy Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - pathology Care and treatment Cell cycle cell cycle arrest Cell Line, Tumor - drug effects Cell Proliferation - drug effects Cyclins - metabolism Drugs, Chinese Herbal - pharmacology Endoplasmic reticulum Endoplasmic Reticulum Stress - drug effects ER stress G1 Phase Cell Cycle Checkpoints - drug effects Gene expression glycyrrhetinic acid Glycyrrhetinic Acid - pharmacology Health aspects Heat-Shock Proteins - metabolism Humans Immunoglobulins Kinases Lung cancer Lung cancer, Non-small cell Lung Neoplasms - drug therapy Lung Neoplasms - metabolism Lung Neoplasms - pathology Medicine, Chinese Membrane Glycoproteins - metabolism NSCLC Phosphorylation - drug effects Protein synthesis Proteins Retinoblastoma Protein - metabolism Transcription factors Variance analysis |
| title | Glycyrrhetinic acid induces G1-phase cell cycle arrest in human non-small cell lung cancer cells through endoplasmic reticulum stress pathway |
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