Up-regulation of p21WAF1 expression in myeloid cells is activated by the protein kinase C pathway
Phorbol-12-myristate-13-acetate (PMA) induces p21WAF-1 expression in human myeloid leukaemic HL-60 cells. We show that this induction is specifically mediated by protein kinase C (PKC). In addition, the PKC inhibitor Ro 31-8220 with predominant PKC-alpha isoform specificity almost completely inhibit...
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| Veröffentlicht in: | British journal of cancer 1997-01, Vol.76 (12), p.1554-1557 |
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| container_title | British journal of cancer |
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| creator | Schwaller, J Peters, UR Pabst, T Niklaus, G Macfarlane, DE Fey, MF Tobler, A |
| description | Phorbol-12-myristate-13-acetate (PMA) induces p21WAF-1 expression in human myeloid leukaemic HL-60 cells. We show that this induction is specifically mediated by protein kinase C (PKC). In addition, the PKC inhibitor Ro 31-8220 with predominant PKC-alpha isoform specificity almost completely inhibited PMA-induced up-regulation of p21WAF1 in HL-60 cells as well as in the myelomonocytic leukaemic U937 cells. Pretreatment of HL-60 cells with Ro 31-8220 also inhibited PMA-induced activation of c-raf-1, a known PKC alpha target. In the phorbol ester-tolerant HL-60 subline (PET) with PKC-beta isoform deficiency PMA or bryostatin-1 induced p21WAF1 expression, but to a lesser extent than in wild-type HL-60 cells. In PET cells, Ro 31-8220 also inhibited PMA and bryostatin-1-induced up-regulation of p21WAF1 expression. Our findings indicate that at least in HL-60 cells up-regulation of p21WAF-1 is specifically activated by PKC. We suggest that PKC isoforms other than beta, presumably the PKC-alpha isoform, are involved in this process. |
| doi_str_mv | 10.1038/bjc.1997.595 |
| format | Article |
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We show that this induction is specifically mediated by protein kinase C (PKC). In addition, the PKC inhibitor Ro 31-8220 with predominant PKC-alpha isoform specificity almost completely inhibited PMA-induced up-regulation of p21WAF1 in HL-60 cells as well as in the myelomonocytic leukaemic U937 cells. Pretreatment of HL-60 cells with Ro 31-8220 also inhibited PMA-induced activation of c-raf-1, a known PKC alpha target. In the phorbol ester-tolerant HL-60 subline (PET) with PKC-beta isoform deficiency PMA or bryostatin-1 induced p21WAF1 expression, but to a lesser extent than in wild-type HL-60 cells. In PET cells, Ro 31-8220 also inhibited PMA and bryostatin-1-induced up-regulation of p21WAF1 expression. Our findings indicate that at least in HL-60 cells up-regulation of p21WAF-1 is specifically activated by PKC. We suggest that PKC isoforms other than beta, presumably the PKC-alpha isoform, are involved in this process.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/bjc.1997.595</identifier><identifier>PMID: 9413940</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins - genetics ; Dose-Response Relationship, Drug ; Drug Resistance ; Epidemiology ; experimental-oncology ; Gene Expression Regulation, Leukemic ; HL-60 Cells ; Humans ; Indoles - pharmacology ; Molecular Medicine ; Oncology ; Phosphorylation ; Protein Kinase C - physiology ; Proto-Oncogene Proteins c-raf - metabolism ; Tetradecanoylphorbol Acetate - pharmacology ; Up-Regulation</subject><ispartof>British journal of cancer, 1997-01, Vol.76 (12), p.1554-1557</ispartof><rights>Cancer Research Campaign 1997</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2645-442a692fbe9b00616b0f01881e5795b98168f91308052544aaa457292aec352f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2228197/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2228197/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,41467,42536,51297,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9413940$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schwaller, J</creatorcontrib><creatorcontrib>Peters, UR</creatorcontrib><creatorcontrib>Pabst, T</creatorcontrib><creatorcontrib>Niklaus, G</creatorcontrib><creatorcontrib>Macfarlane, DE</creatorcontrib><creatorcontrib>Fey, MF</creatorcontrib><creatorcontrib>Tobler, A</creatorcontrib><title>Up-regulation of p21WAF1 expression in myeloid cells is activated by the protein kinase C pathway</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Phorbol-12-myristate-13-acetate (PMA) induces p21WAF-1 expression in human myeloid leukaemic HL-60 cells. We show that this induction is specifically mediated by protein kinase C (PKC). In addition, the PKC inhibitor Ro 31-8220 with predominant PKC-alpha isoform specificity almost completely inhibited PMA-induced up-regulation of p21WAF1 in HL-60 cells as well as in the myelomonocytic leukaemic U937 cells. Pretreatment of HL-60 cells with Ro 31-8220 also inhibited PMA-induced activation of c-raf-1, a known PKC alpha target. In the phorbol ester-tolerant HL-60 subline (PET) with PKC-beta isoform deficiency PMA or bryostatin-1 induced p21WAF1 expression, but to a lesser extent than in wild-type HL-60 cells. In PET cells, Ro 31-8220 also inhibited PMA and bryostatin-1-induced up-regulation of p21WAF1 expression. Our findings indicate that at least in HL-60 cells up-regulation of p21WAF-1 is specifically activated by PKC. We suggest that PKC isoforms other than beta, presumably the PKC-alpha isoform, are involved in this process.</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cyclin-Dependent Kinase Inhibitor p21</subject><subject>Cyclins - genetics</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>experimental-oncology</subject><subject>Gene Expression Regulation, Leukemic</subject><subject>HL-60 Cells</subject><subject>Humans</subject><subject>Indoles - pharmacology</subject><subject>Molecular Medicine</subject><subject>Oncology</subject><subject>Phosphorylation</subject><subject>Protein Kinase C - physiology</subject><subject>Proto-Oncogene Proteins c-raf - metabolism</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><subject>Up-Regulation</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkNFKwzAUhoMoc07vvBXyAHYmadImN8IYToWBNw4vQ9qdbpldU5Juurc3Y2MoeBVOvv_8Bz6EbikZUpLKh2JVDqlS-VAocYb6VKQsoZLl56hPCMkTohi5RFchrOKoiMx7qKc4TRUnfWRmbeJhsalNZ12DXYVbRj9GE4rhu_UQwv7XNni9g9rZOS6hrgO2AZuys1vTwRwXO9wtAbfedRCTn7YxAfAYt6ZbfpndNbqoTB3g5vgO0Gzy9D5-SaZvz6_j0TQpWcZFwjkzmWJVAaogJKNZQSpCpaQgciUKJWkmK0VTIolggnNjDBc5U8xAmQpWpQP0eOhtN8Ua5iU0nTe1br1dG7_Tzlj9lzR2qRduqxljkqo8FtwfCkrvQvBQnXYp0XvTOprWe9M6mo7xu9_3TuGj2siTAw-RNAvweuU2vokK_u_7AXjbiK0</recordid><startdate>19970101</startdate><enddate>19970101</enddate><creator>Schwaller, J</creator><creator>Peters, UR</creator><creator>Pabst, T</creator><creator>Niklaus, G</creator><creator>Macfarlane, DE</creator><creator>Fey, MF</creator><creator>Tobler, A</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>5PM</scope></search><sort><creationdate>19970101</creationdate><title>Up-regulation of p21WAF1 expression in myeloid cells is activated by the protein kinase C pathway</title><author>Schwaller, J ; Peters, UR ; Pabst, T ; Niklaus, G ; Macfarlane, DE ; Fey, MF ; Tobler, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2645-442a692fbe9b00616b0f01881e5795b98168f91308052544aaa457292aec352f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Cyclin-Dependent Kinase Inhibitor p21</topic><topic>Cyclins - genetics</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Resistance</topic><topic>Epidemiology</topic><topic>experimental-oncology</topic><topic>Gene Expression Regulation, Leukemic</topic><topic>HL-60 Cells</topic><topic>Humans</topic><topic>Indoles - pharmacology</topic><topic>Molecular Medicine</topic><topic>Oncology</topic><topic>Phosphorylation</topic><topic>Protein Kinase C - physiology</topic><topic>Proto-Oncogene Proteins c-raf - metabolism</topic><topic>Tetradecanoylphorbol Acetate - pharmacology</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schwaller, J</creatorcontrib><creatorcontrib>Peters, UR</creatorcontrib><creatorcontrib>Pabst, T</creatorcontrib><creatorcontrib>Niklaus, G</creatorcontrib><creatorcontrib>Macfarlane, DE</creatorcontrib><creatorcontrib>Fey, MF</creatorcontrib><creatorcontrib>Tobler, A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schwaller, J</au><au>Peters, UR</au><au>Pabst, T</au><au>Niklaus, G</au><au>Macfarlane, DE</au><au>Fey, MF</au><au>Tobler, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Up-regulation of p21WAF1 expression in myeloid cells is activated by the protein kinase C pathway</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>1997-01-01</date><risdate>1997</risdate><volume>76</volume><issue>12</issue><spage>1554</spage><epage>1557</epage><pages>1554-1557</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><abstract>Phorbol-12-myristate-13-acetate (PMA) induces p21WAF-1 expression in human myeloid leukaemic HL-60 cells. We show that this induction is specifically mediated by protein kinase C (PKC). In addition, the PKC inhibitor Ro 31-8220 with predominant PKC-alpha isoform specificity almost completely inhibited PMA-induced up-regulation of p21WAF1 in HL-60 cells as well as in the myelomonocytic leukaemic U937 cells. Pretreatment of HL-60 cells with Ro 31-8220 also inhibited PMA-induced activation of c-raf-1, a known PKC alpha target. In the phorbol ester-tolerant HL-60 subline (PET) with PKC-beta isoform deficiency PMA or bryostatin-1 induced p21WAF1 expression, but to a lesser extent than in wild-type HL-60 cells. In PET cells, Ro 31-8220 also inhibited PMA and bryostatin-1-induced up-regulation of p21WAF1 expression. Our findings indicate that at least in HL-60 cells up-regulation of p21WAF-1 is specifically activated by PKC. We suggest that PKC isoforms other than beta, presumably the PKC-alpha isoform, are involved in this process.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>9413940</pmid><doi>10.1038/bjc.1997.595</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Nature; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; SpringerLink Journals - AutoHoldings |
| subjects | Biomedical and Life Sciences Biomedicine Cancer Research Cyclin-Dependent Kinase Inhibitor p21 Cyclins - genetics Dose-Response Relationship, Drug Drug Resistance Epidemiology experimental-oncology Gene Expression Regulation, Leukemic HL-60 Cells Humans Indoles - pharmacology Molecular Medicine Oncology Phosphorylation Protein Kinase C - physiology Proto-Oncogene Proteins c-raf - metabolism Tetradecanoylphorbol Acetate - pharmacology Up-Regulation |
| title | Up-regulation of p21WAF1 expression in myeloid cells is activated by the protein kinase C pathway |
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