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Pectenotoxin-2 represses telomerase activity in human leukemia cells through suppression of hTERT gene expression and Akt-dependent hTERT phosphorylation
In this study, we found that pectenotoxin-2 (PTX-2) decreased cell viability and inhibited telomerase activity with downregulation of hTERT expression in human leukemia cells. PTX-2 treatment also reduced c-Myc and Sp1 gene expression and DNA binding activity. Further chromatin immunoprecipitation a...
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| Published in: | FEBS letters 2008-10, Vol.582 (23-24), p.3263-3269 |
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| Main Authors: | , , , , , , , |
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| cited_by | cdi_FETCH-LOGICAL-c5725-a91ebd594c6e93d90b401928530d7072d7058cb3f486a62ffc2c5b594cec8e7f3 |
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| cites | cdi_FETCH-LOGICAL-c5725-a91ebd594c6e93d90b401928530d7072d7058cb3f486a62ffc2c5b594cec8e7f3 |
| container_end_page | 3269 |
| container_issue | 23-24 |
| container_start_page | 3263 |
| container_title | FEBS letters |
| container_volume | 582 |
| creator | Kim, Mun-Ock Moon, Dong-Oh Kang, Sang-Hyuck Heo, Moon-Soo Choi, Yung Hyun Jung, Jee Hyung Lee, Jae-Dong Kim, Gi-Young |
| description | In this study, we found that pectenotoxin-2 (PTX-2) decreased cell viability and inhibited telomerase activity with downregulation of hTERT expression in human leukemia cells. PTX-2 treatment also reduced c-Myc and Sp1 gene expression and DNA binding activity. Further chromatin immunoprecipitation assay demonstrated that PTX-2 attenuated the binding of c-Myc and Sp1 to the regulatory regions of hTERT. We also observed that PTX-2 treatment attenuated the phosphorylation of Akt, thereby reducing the phosphorylation and nuclear translocation of hTERT. We concluded that PTX-2 suppressed telomerase activity through the transcriptional and post-translational suppression of hTERT and this process precedes cellular differentiation of human leukemia cells.
MINT-6742762:hTERT (uniprotkb:O14746) physically interacts (MI:0218) with AKT (uniprotkb:P31749) by anti bait coimmunoprecipitation (MI:0006) |
| doi_str_mv | 10.1016/j.febslet.2008.08.030 |
| format | article |
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MINT-6742762:hTERT (uniprotkb:O14746) physically interacts (MI:0218) with AKT (uniprotkb:P31749) by anti bait coimmunoprecipitation (MI:0006)</description><identifier>ISSN: 0014-5793</identifier><identifier>EISSN: 1873-3468</identifier><identifier>DOI: 10.1016/j.febslet.2008.08.030</identifier><identifier>PMID: 18775701</identifier><language>eng</language><publisher>England: Elsevier B.V</publisher><subject>Akt ; Apoptosis ; c-Myc ; Cell Line, Tumor ; Cell Proliferation - drug effects ; ChIP ; Chromatin Immunoprecipitation ; DNA repair enzyme poly-(ADP-ribose) polymerase ; ELISA ; enzyme-linked immunosorbent assay ; Furans - pharmacology ; Gene Expression - drug effects ; hTERT ; Humans ; Leukemia - metabolism ; PARP ; Pectenotoxin-2 ; Phosphorylation - drug effects ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-myc - metabolism ; PTX-2 ; Pyrans - pharmacology ; Sp1 ; Sp1 Transcription Factor - metabolism ; Telomerase - antagonists & inhibitors ; Telomerase - genetics ; telomeric repeat amplification protocol ; TRAP</subject><ispartof>FEBS letters, 2008-10, Vol.582 (23-24), p.3263-3269</ispartof><rights>2008</rights><rights>FEBS Letters 582 (2008) 1873-3468 © 2015 Federation of European Biochemical Societies</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5725-a91ebd594c6e93d90b401928530d7072d7058cb3f486a62ffc2c5b594cec8e7f3</citedby><cites>FETCH-LOGICAL-c5725-a91ebd594c6e93d90b401928530d7072d7058cb3f486a62ffc2c5b594cec8e7f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0014579308007175$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,778,782,3538,27907,27908,45763</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18775701$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Mun-Ock</creatorcontrib><creatorcontrib>Moon, Dong-Oh</creatorcontrib><creatorcontrib>Kang, Sang-Hyuck</creatorcontrib><creatorcontrib>Heo, Moon-Soo</creatorcontrib><creatorcontrib>Choi, Yung Hyun</creatorcontrib><creatorcontrib>Jung, Jee Hyung</creatorcontrib><creatorcontrib>Lee, Jae-Dong</creatorcontrib><creatorcontrib>Kim, Gi-Young</creatorcontrib><title>Pectenotoxin-2 represses telomerase activity in human leukemia cells through suppression of hTERT gene expression and Akt-dependent hTERT phosphorylation</title><title>FEBS letters</title><addtitle>FEBS Lett</addtitle><description>In this study, we found that pectenotoxin-2 (PTX-2) decreased cell viability and inhibited telomerase activity with downregulation of hTERT expression in human leukemia cells. PTX-2 treatment also reduced c-Myc and Sp1 gene expression and DNA binding activity. Further chromatin immunoprecipitation assay demonstrated that PTX-2 attenuated the binding of c-Myc and Sp1 to the regulatory regions of hTERT. We also observed that PTX-2 treatment attenuated the phosphorylation of Akt, thereby reducing the phosphorylation and nuclear translocation of hTERT. We concluded that PTX-2 suppressed telomerase activity through the transcriptional and post-translational suppression of hTERT and this process precedes cellular differentiation of human leukemia cells.
MINT-6742762:hTERT (uniprotkb:O14746) physically interacts (MI:0218) with AKT (uniprotkb:P31749) by anti bait coimmunoprecipitation (MI:0006)</description><subject>Akt</subject><subject>Apoptosis</subject><subject>c-Myc</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>ChIP</subject><subject>Chromatin Immunoprecipitation</subject><subject>DNA repair enzyme poly-(ADP-ribose) polymerase</subject><subject>ELISA</subject><subject>enzyme-linked immunosorbent assay</subject><subject>Furans - pharmacology</subject><subject>Gene Expression - drug effects</subject><subject>hTERT</subject><subject>Humans</subject><subject>Leukemia - metabolism</subject><subject>PARP</subject><subject>Pectenotoxin-2</subject><subject>Phosphorylation - drug effects</subject><subject>Proto-Oncogene Proteins c-akt</subject><subject>Proto-Oncogene Proteins c-myc - metabolism</subject><subject>PTX-2</subject><subject>Pyrans - pharmacology</subject><subject>Sp1</subject><subject>Sp1 Transcription Factor - metabolism</subject><subject>Telomerase - antagonists & inhibitors</subject><subject>Telomerase - genetics</subject><subject>telomeric repeat amplification protocol</subject><subject>TRAP</subject><issn>0014-5793</issn><issn>1873-3468</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNqNkttu1DAQhiMEokvhEUC-4i6LD0nsXKFSbSlSJRAs15bjTBpvEzvYTuk-Cm-Lw0ZwWaSxR5a_-X34J8teE7wlmFTvDtsOmjBA3FKMxXYJhp9kGyI4y1lRiafZBmNS5CWv2Vn2IoQDTmtB6ufZWYJ4yTHZZL--gI5gXXQPxuYUeZg8hAABRRjcCF4FQEpHc2_iERmL-nlUFg0w38FoFNIwDIntvZtvexTm6U-5cRa5DvX73dc9ugULCB7-bijboou7mLcwgW3BxpWbehfS8MdBxcS9zJ51agjwas3n2fer3f7yOr_5_PHT5cVNrktOy1zVBJq2rAtdQc3aGjcFJjUVJcMtx5ymqRS6YV0hKlXRrtNUl83CgxbAO3aevT3pTt79mCFEOZqwPEtZcHOQVc0LygR9FCQ1J4IWPIHlCdTeheChk5M3o_JHSbBczJMHuZonF_PkEgynujfrAXMzQvuvanUrAdcn4KcZ4Ph_qvJq94F-WzphaQQsMOaEl0nq_UkK0tfeG_AyaANWQ2t86gjZOvPIbX8DkG7Gyg</recordid><startdate>20081015</startdate><enddate>20081015</enddate><creator>Kim, Mun-Ock</creator><creator>Moon, Dong-Oh</creator><creator>Kang, Sang-Hyuck</creator><creator>Heo, Moon-Soo</creator><creator>Choi, Yung Hyun</creator><creator>Jung, Jee Hyung</creator><creator>Lee, Jae-Dong</creator><creator>Kim, Gi-Young</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</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>7QO</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20081015</creationdate><title>Pectenotoxin-2 represses telomerase activity in human leukemia cells through suppression of hTERT gene expression and Akt-dependent hTERT phosphorylation</title><author>Kim, Mun-Ock ; Moon, Dong-Oh ; Kang, Sang-Hyuck ; Heo, Moon-Soo ; Choi, Yung Hyun ; Jung, Jee Hyung ; Lee, Jae-Dong ; Kim, Gi-Young</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5725-a91ebd594c6e93d90b401928530d7072d7058cb3f486a62ffc2c5b594cec8e7f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Akt</topic><topic>Apoptosis</topic><topic>c-Myc</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>ChIP</topic><topic>Chromatin Immunoprecipitation</topic><topic>DNA repair enzyme poly-(ADP-ribose) polymerase</topic><topic>ELISA</topic><topic>enzyme-linked immunosorbent assay</topic><topic>Furans - pharmacology</topic><topic>Gene Expression - drug effects</topic><topic>hTERT</topic><topic>Humans</topic><topic>Leukemia - metabolism</topic><topic>PARP</topic><topic>Pectenotoxin-2</topic><topic>Phosphorylation - drug effects</topic><topic>Proto-Oncogene Proteins c-akt</topic><topic>Proto-Oncogene Proteins c-myc - metabolism</topic><topic>PTX-2</topic><topic>Pyrans - pharmacology</topic><topic>Sp1</topic><topic>Sp1 Transcription Factor - metabolism</topic><topic>Telomerase - antagonists & inhibitors</topic><topic>Telomerase - genetics</topic><topic>telomeric repeat amplification protocol</topic><topic>TRAP</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Mun-Ock</creatorcontrib><creatorcontrib>Moon, Dong-Oh</creatorcontrib><creatorcontrib>Kang, Sang-Hyuck</creatorcontrib><creatorcontrib>Heo, Moon-Soo</creatorcontrib><creatorcontrib>Choi, Yung Hyun</creatorcontrib><creatorcontrib>Jung, Jee Hyung</creatorcontrib><creatorcontrib>Lee, Jae-Dong</creatorcontrib><creatorcontrib>Kim, Gi-Young</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Nucleic Acids Abstracts</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>FEBS letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Mun-Ock</au><au>Moon, Dong-Oh</au><au>Kang, Sang-Hyuck</au><au>Heo, Moon-Soo</au><au>Choi, Yung Hyun</au><au>Jung, Jee Hyung</au><au>Lee, Jae-Dong</au><au>Kim, Gi-Young</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pectenotoxin-2 represses telomerase activity in human leukemia cells through suppression of hTERT gene expression and Akt-dependent hTERT phosphorylation</atitle><jtitle>FEBS letters</jtitle><addtitle>FEBS Lett</addtitle><date>2008-10-15</date><risdate>2008</risdate><volume>582</volume><issue>23-24</issue><spage>3263</spage><epage>3269</epage><pages>3263-3269</pages><issn>0014-5793</issn><eissn>1873-3468</eissn><abstract>In this study, we found that pectenotoxin-2 (PTX-2) decreased cell viability and inhibited telomerase activity with downregulation of hTERT expression in human leukemia cells. PTX-2 treatment also reduced c-Myc and Sp1 gene expression and DNA binding activity. Further chromatin immunoprecipitation assay demonstrated that PTX-2 attenuated the binding of c-Myc and Sp1 to the regulatory regions of hTERT. We also observed that PTX-2 treatment attenuated the phosphorylation of Akt, thereby reducing the phosphorylation and nuclear translocation of hTERT. We concluded that PTX-2 suppressed telomerase activity through the transcriptional and post-translational suppression of hTERT and this process precedes cellular differentiation of human leukemia cells.
MINT-6742762:hTERT (uniprotkb:O14746) physically interacts (MI:0218) with AKT (uniprotkb:P31749) by anti bait coimmunoprecipitation (MI:0006)</abstract><cop>England</cop><pub>Elsevier B.V</pub><pmid>18775701</pmid><doi>10.1016/j.febslet.2008.08.030</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0014-5793 |
| ispartof | FEBS letters, 2008-10, Vol.582 (23-24), p.3263-3269 |
| issn | 0014-5793 1873-3468 |
| language | eng |
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| source | ScienceDirect Journals; Wiley-Blackwell Read & Publish Collection |
| subjects | Akt Apoptosis c-Myc Cell Line, Tumor Cell Proliferation - drug effects ChIP Chromatin Immunoprecipitation DNA repair enzyme poly-(ADP-ribose) polymerase ELISA enzyme-linked immunosorbent assay Furans - pharmacology Gene Expression - drug effects hTERT Humans Leukemia - metabolism PARP Pectenotoxin-2 Phosphorylation - drug effects Proto-Oncogene Proteins c-akt Proto-Oncogene Proteins c-myc - metabolism PTX-2 Pyrans - pharmacology Sp1 Sp1 Transcription Factor - metabolism Telomerase - antagonists & inhibitors Telomerase - genetics telomeric repeat amplification protocol TRAP |
| title | Pectenotoxin-2 represses telomerase activity in human leukemia cells through suppression of hTERT gene expression and Akt-dependent hTERT phosphorylation |
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