Piperlongumine reverses doxorubicin resistance through the PI3K/Akt signaling pathway in K562/A02 human leukemia cells
Drug resistance is an important obstacle to human leukemia therapeutics. Piperlongumine has previously demonstrated the ability to suppress certain human tumor processes; however, the ability of piperlongumine to reverse the drug resistance of human leukemia and its mechanism of action have not yet...
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| Veröffentlicht in: | Experimental and therapeutic medicine 2015-04, Vol.9 (4), p.1345-1350 |
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| description | Drug resistance is an important obstacle to human leukemia therapeutics. Piperlongumine has previously demonstrated the ability to suppress certain human tumor processes; however, the ability of piperlongumine to reverse the drug resistance of human leukemia and its mechanism of action have not yet been clearly elucidated. In this study, the doxorubicin resistance reversal effect of piperlongumine on K562/A02 human leukemia cells and the underlying mechanism were investigated. The results indicated that piperlongumine promoted doxorubicin sensitivity, apoptosis, the intracellular accumulation of rhodamine-123, the activities of caspase-3 and -8, and the expression of reactive oxygen species, p53, p27 and p-PTEN. Furthermore, it suppressed the expression of P-glycoprotein, MDR1, MRP1, survivin and p-Akt, and the transcriptional activities of NF-κB and twist, and arrested the cell cycle in the G2/M phase. The results indicate that piperlongumine has the potential to be used as a therapeutic agent for human leukemia. |
| doi_str_mv | 10.3892/etm.2015.2254 |
| format | Article |
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Piperlongumine has previously demonstrated the ability to suppress certain human tumor processes; however, the ability of piperlongumine to reverse the drug resistance of human leukemia and its mechanism of action have not yet been clearly elucidated. In this study, the doxorubicin resistance reversal effect of piperlongumine on K562/A02 human leukemia cells and the underlying mechanism were investigated. The results indicated that piperlongumine promoted doxorubicin sensitivity, apoptosis, the intracellular accumulation of rhodamine-123, the activities of caspase-3 and -8, and the expression of reactive oxygen species, p53, p27 and p-PTEN. Furthermore, it suppressed the expression of P-glycoprotein, MDR1, MRP1, survivin and p-Akt, and the transcriptional activities of NF-κB and twist, and arrested the cell cycle in the G2/M phase. The results indicate that piperlongumine has the potential to be used as a therapeutic agent for human leukemia.</description><identifier>ISSN: 1792-0981</identifier><identifier>EISSN: 1792-1015</identifier><identifier>DOI: 10.3892/etm.2015.2254</identifier><identifier>PMID: 25780433</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Antimitotic agents ; Antineoplastic agents ; Apoptosis ; Bone marrow ; Care and treatment ; Cell cycle ; doxorubicin resistance ; Drug resistance ; Flow cytometry ; Gene expression ; human leukemia ; Kinases ; Leukemia ; Medical research ; Medicine, Experimental ; Phosphorylation ; piperlongumine ; Polymerase chain reaction ; Reactive oxygen species ; Signal transduction ; Stem cells</subject><ispartof>Experimental and therapeutic medicine, 2015-04, Vol.9 (4), p.1345-1350</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-c514t-1f9643290e26447b0a965771d4d3075c4df39382b1d8b05a25e62d418ac6d46b3</citedby><cites>FETCH-LOGICAL-c514t-1f9643290e26447b0a965771d4d3075c4df39382b1d8b05a25e62d418ac6d46b3</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/PMC4353808/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4353808/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25780433$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KANG, QINGWEI</creatorcontrib><creatorcontrib>YAN, SHU</creatorcontrib><title>Piperlongumine reverses doxorubicin resistance through the PI3K/Akt signaling pathway in K562/A02 human leukemia cells</title><title>Experimental and therapeutic medicine</title><addtitle>Exp Ther Med</addtitle><description>Drug resistance is an important obstacle to human leukemia therapeutics. Piperlongumine has previously demonstrated the ability to suppress certain human tumor processes; however, the ability of piperlongumine to reverse the drug resistance of human leukemia and its mechanism of action have not yet been clearly elucidated. In this study, the doxorubicin resistance reversal effect of piperlongumine on K562/A02 human leukemia cells and the underlying mechanism were investigated. The results indicated that piperlongumine promoted doxorubicin sensitivity, apoptosis, the intracellular accumulation of rhodamine-123, the activities of caspase-3 and -8, and the expression of reactive oxygen species, p53, p27 and p-PTEN. Furthermore, it suppressed the expression of P-glycoprotein, MDR1, MRP1, survivin and p-Akt, and the transcriptional activities of NF-κB and twist, and arrested the cell cycle in the G2/M phase. The results indicate that piperlongumine has the potential to be used as a therapeutic agent for human leukemia.</description><subject>Antimitotic agents</subject><subject>Antineoplastic agents</subject><subject>Apoptosis</subject><subject>Bone marrow</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>doxorubicin resistance</subject><subject>Drug resistance</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>human leukemia</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Phosphorylation</subject><subject>piperlongumine</subject><subject>Polymerase chain reaction</subject><subject>Reactive oxygen species</subject><subject>Signal transduction</subject><subject>Stem cells</subject><issn>1792-0981</issn><issn>1792-1015</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptkk1v1DAQhiMEolXpkSuKxAEu2fV3nAvSqoJStRI9wNly4kniNrEXO9nSf19HuywUYR9mNH7mtWb0ZtlbjFZUVmQN07giCPMVIZy9yE5xWZECp8LLQ44qiU-y8xjvUDpcYCn56-yE8FIiRulptru1WwiDd908Wgd5gB2ECDE3_pcPc20b61Ix2jhp10A-9cHPXZ8i5LdX9Hq9uZ_yaDunB-u6fKun_kE_5qnpmguy3iCS9_OoXT7AfA-j1XkDwxDfZK9aPUQ4P8Sz7MeXz98vvhY33y6vLjY3RcMxmwrcVoJRUiEggrGyRroSvCyxYYaikjfMtLSiktTYyBpxTTgIYhiWuhGGiZqeZZ_2utu5HsE04KagB7UNdtThUXlt1fMXZ3vV-Z1ilFOJZBL4eBAI_ucMcVKjjcsI2oGfo8KSCEEYRmVC3_-D3vk5pMUkqqIYUcZE9Yfq9ADKutanf5tFVG0YkqVMA5FErf5DpWvSDhvvoLWp_qyh2Dc0wccYoD3OiJFavKKSV9TiFbV4JfHv_l7Mkf7tjAR82ANxq52xxscjk5SSsQrECkwZp0_o1cVz</recordid><startdate>20150401</startdate><enddate>20150401</enddate><creator>KANG, QINGWEI</creator><creator>YAN, SHU</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</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>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150401</creationdate><title>Piperlongumine reverses doxorubicin resistance through the PI3K/Akt signaling pathway in K562/A02 human leukemia cells</title><author>KANG, QINGWEI ; YAN, SHU</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-1f9643290e26447b0a965771d4d3075c4df39382b1d8b05a25e62d418ac6d46b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Antimitotic agents</topic><topic>Antineoplastic agents</topic><topic>Apoptosis</topic><topic>Bone marrow</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>doxorubicin resistance</topic><topic>Drug resistance</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>human leukemia</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Medical research</topic><topic>Medicine, Experimental</topic><topic>Phosphorylation</topic><topic>piperlongumine</topic><topic>Polymerase chain reaction</topic><topic>Reactive oxygen species</topic><topic>Signal transduction</topic><topic>Stem cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KANG, QINGWEI</creatorcontrib><creatorcontrib>YAN, SHU</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Experimental and therapeutic medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KANG, QINGWEI</au><au>YAN, SHU</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Piperlongumine reverses doxorubicin resistance through the PI3K/Akt signaling pathway in K562/A02 human leukemia cells</atitle><jtitle>Experimental and therapeutic medicine</jtitle><addtitle>Exp Ther Med</addtitle><date>2015-04-01</date><risdate>2015</risdate><volume>9</volume><issue>4</issue><spage>1345</spage><epage>1350</epage><pages>1345-1350</pages><issn>1792-0981</issn><eissn>1792-1015</eissn><abstract>Drug resistance is an important obstacle to human leukemia therapeutics. Piperlongumine has previously demonstrated the ability to suppress certain human tumor processes; however, the ability of piperlongumine to reverse the drug resistance of human leukemia and its mechanism of action have not yet been clearly elucidated. In this study, the doxorubicin resistance reversal effect of piperlongumine on K562/A02 human leukemia cells and the underlying mechanism were investigated. The results indicated that piperlongumine promoted doxorubicin sensitivity, apoptosis, the intracellular accumulation of rhodamine-123, the activities of caspase-3 and -8, and the expression of reactive oxygen species, p53, p27 and p-PTEN. Furthermore, it suppressed the expression of P-glycoprotein, MDR1, MRP1, survivin and p-Akt, and the transcriptional activities of NF-κB and twist, and arrested the cell cycle in the G2/M phase. The results indicate that piperlongumine has the potential to be used as a therapeutic agent for human leukemia.</abstract><cop>Greece</cop><pub>D.A. 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| subjects | Antimitotic agents Antineoplastic agents Apoptosis Bone marrow Care and treatment Cell cycle doxorubicin resistance Drug resistance Flow cytometry Gene expression human leukemia Kinases Leukemia Medical research Medicine, Experimental Phosphorylation piperlongumine Polymerase chain reaction Reactive oxygen species Signal transduction Stem cells |
| title | Piperlongumine reverses doxorubicin resistance through the PI3K/Akt signaling pathway in K562/A02 human leukemia cells |
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