Extracellular NM23 protein promotes the growth and survival of primary cultured human acute myelogenous leukemia cells
An elevated serum level of NM23‐H1 protein is found in acute myelogenous leukemia (AML), and predicts a poor treatment outcome in AML patients. To investigate the potential pathological link between the elevated serum level of this protein and poor prognosis, we examined the extracellular effects of...
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| Veröffentlicht in: | Cancer science 2009-10, Vol.100 (10), p.1885-1894 |
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| creator | Okabe‐Kado, Junko Kasukabe, Takashi Honma, Yoshio Kobayashi, Hirofumi Maseki, Nobuo Kaneko, Yasuhiko |
| description | An elevated serum level of NM23‐H1 protein is found in acute myelogenous leukemia (AML), and predicts a poor treatment outcome in AML patients. To investigate the potential pathological link between the elevated serum level of this protein and poor prognosis, we examined the extracellular effects of recombinant NM23‐H1 protein on the in vitro growth and survival of primary cultured AML cells at concentrations equivalent to the levels found in the serum of AML patients. Extracellular NM23‐H1 protein promoted the in vitro growth and survival of AML cells and this activity was associated with the cytokine production and activation of the MAPK and signal transducers and activators of transcription signaling pathways. Inhibitors specific to MAPK signaling pathways inhibited the growth‐ and survival‐promoting activity of NM23‐H1. These findings indicate the novel biological action of extracellular NM23‐H1 and its association with poor prognosis, and suggest an important role for extracellular NM23‐H1 in the malignant progression of leukemia and a potential therapeutic target for these malignancies. (Cancer Sci 2009; 100: 1885–1894) |
| doi_str_mv | 10.1111/j.1349-7006.2009.01276.x |
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To investigate the potential pathological link between the elevated serum level of this protein and poor prognosis, we examined the extracellular effects of recombinant NM23‐H1 protein on the in vitro growth and survival of primary cultured AML cells at concentrations equivalent to the levels found in the serum of AML patients. Extracellular NM23‐H1 protein promoted the in vitro growth and survival of AML cells and this activity was associated with the cytokine production and activation of the MAPK and signal transducers and activators of transcription signaling pathways. Inhibitors specific to MAPK signaling pathways inhibited the growth‐ and survival‐promoting activity of NM23‐H1. These findings indicate the novel biological action of extracellular NM23‐H1 and its association with poor prognosis, and suggest an important role for extracellular NM23‐H1 in the malignant progression of leukemia and a potential therapeutic target for these malignancies. 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Myelofibrosis ; Medical sciences ; NM23 Nucleoside Diphosphate Kinases - genetics ; NM23 Nucleoside Diphosphate Kinases - metabolism ; Original ; Prognosis ; Recombinant Proteins - genetics ; Recombinant Proteins - metabolism ; Signal Transduction - physiology ; Tumors</subject><ispartof>Cancer science, 2009-10, Vol.100 (10), p.1885-1894</ispartof><rights>2009 Japanese Cancer Association</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6536-b07405081627456e0bb6816efa5f012e4d12c216be2157e9efa1c30b4e6418bc3</citedby><cites>FETCH-LOGICAL-c6536-b07405081627456e0bb6816efa5f012e4d12c216be2157e9efa1c30b4e6418bc3</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/PMC11158594/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11158594/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1349-7006.2009.01276.x$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21975970$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19664043$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Okabe‐Kado, Junko</creatorcontrib><creatorcontrib>Kasukabe, Takashi</creatorcontrib><creatorcontrib>Honma, Yoshio</creatorcontrib><creatorcontrib>Kobayashi, Hirofumi</creatorcontrib><creatorcontrib>Maseki, Nobuo</creatorcontrib><creatorcontrib>Kaneko, Yasuhiko</creatorcontrib><title>Extracellular NM23 protein promotes the growth and survival of primary cultured human acute myelogenous leukemia cells</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>An elevated serum level of NM23‐H1 protein is found in acute myelogenous leukemia (AML), and predicts a poor treatment outcome in AML patients. To investigate the potential pathological link between the elevated serum level of this protein and poor prognosis, we examined the extracellular effects of recombinant NM23‐H1 protein on the in vitro growth and survival of primary cultured AML cells at concentrations equivalent to the levels found in the serum of AML patients. Extracellular NM23‐H1 protein promoted the in vitro growth and survival of AML cells and this activity was associated with the cytokine production and activation of the MAPK and signal transducers and activators of transcription signaling pathways. Inhibitors specific to MAPK signaling pathways inhibited the growth‐ and survival‐promoting activity of NM23‐H1. These findings indicate the novel biological action of extracellular NM23‐H1 and its association with poor prognosis, and suggest an important role for extracellular NM23‐H1 in the malignant progression of leukemia and a potential therapeutic target for these malignancies. (Cancer Sci 2009; 100: 1885–1894)</description><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - analysis</subject><subject>Blotting, Western</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cell Survival - physiology</subject><subject>Cytokines - metabolism</subject><subject>Extracellular Fluid - chemistry</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Leukemia, Myeloid, Acute - genetics</subject><subject>Leukemia, Myeloid, Acute - metabolism</subject><subject>Leukemia, Myeloid, Acute - pathology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical sciences</subject><subject>NM23 Nucleoside Diphosphate Kinases - genetics</subject><subject>NM23 Nucleoside Diphosphate Kinases - metabolism</subject><subject>Original</subject><subject>Prognosis</subject><subject>Recombinant Proteins - genetics</subject><subject>Recombinant Proteins - metabolism</subject><subject>Signal Transduction - physiology</subject><subject>Tumors</subject><issn>1347-9032</issn><issn>1349-7006</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1v1DAQhiMEoqXwF5AvcEvq78QHhKpVC5VKOQBny_FOdrM4SbHj7e6_x-lG23KivsxY83hmXr9ZhgguSDrnm4IwrvISY1lQjFWBCS1lsXuRnR4LLx_yMleY0ZPsTQgbjJnkir_OToiSkmPOTrPt5W70xoJz0RmPbr9Rhu78MELbT7FLWUDjGtDKD_fjGpl-iUL023ZrHBqaxLSd8XtkoxujhyVax870yNg4Aur24IYV9EMMyEH8DV1r0DQrvM1eNcYFeDfHs-zX1eXPxdf85vuX68XFTW6lYDKvccmxwBWRtORCAq5rmS7QGNEkycCXhFpKZA2UiBJUKhDLcM1BclLVlp1lnw9972LdwdJCn9Q6PW-tB9Pqfyt9u9arYavTL4tKKJ46fJw7-OFPhDDqrg2TBtND0qVlKYUSmPwXpLiiFWcqgdUBtH4IwUNzXIfgaS7RGz25qCcX9WSvfrBX79LT90_lPD6c_UzAhxkwwRrXeNPbNhw5SlQpVIkT9-nA3bcO9s9eQC8ufkwZ-wsDE8M9</recordid><startdate>200910</startdate><enddate>200910</enddate><creator>Okabe‐Kado, Junko</creator><creator>Kasukabe, Takashi</creator><creator>Honma, Yoshio</creator><creator>Kobayashi, Hirofumi</creator><creator>Maseki, Nobuo</creator><creator>Kaneko, Yasuhiko</creator><general>Blackwell Publishing Asia</general><general>Blackwell</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>7T5</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200910</creationdate><title>Extracellular NM23 protein promotes the growth and survival of primary cultured human acute myelogenous leukemia cells</title><author>Okabe‐Kado, Junko ; Kasukabe, Takashi ; Honma, Yoshio ; Kobayashi, Hirofumi ; Maseki, Nobuo ; Kaneko, Yasuhiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6536-b07405081627456e0bb6816efa5f012e4d12c216be2157e9efa1c30b4e6418bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - analysis</topic><topic>Blotting, Western</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cell Survival - physiology</topic><topic>Cytokines - metabolism</topic><topic>Extracellular Fluid - chemistry</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Leukemia, Myeloid, Acute - genetics</topic><topic>Leukemia, Myeloid, Acute - metabolism</topic><topic>Leukemia, Myeloid, Acute - pathology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>NM23 Nucleoside Diphosphate Kinases - genetics</topic><topic>NM23 Nucleoside Diphosphate Kinases - metabolism</topic><topic>Original</topic><topic>Prognosis</topic><topic>Recombinant Proteins - genetics</topic><topic>Recombinant Proteins - metabolism</topic><topic>Signal Transduction - physiology</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Okabe‐Kado, Junko</creatorcontrib><creatorcontrib>Kasukabe, Takashi</creatorcontrib><creatorcontrib>Honma, Yoshio</creatorcontrib><creatorcontrib>Kobayashi, Hirofumi</creatorcontrib><creatorcontrib>Maseki, Nobuo</creatorcontrib><creatorcontrib>Kaneko, Yasuhiko</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Okabe‐Kado, Junko</au><au>Kasukabe, Takashi</au><au>Honma, Yoshio</au><au>Kobayashi, Hirofumi</au><au>Maseki, Nobuo</au><au>Kaneko, Yasuhiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Extracellular NM23 protein promotes the growth and survival of primary cultured human acute myelogenous leukemia cells</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2009-10</date><risdate>2009</risdate><volume>100</volume><issue>10</issue><spage>1885</spage><epage>1894</epage><pages>1885-1894</pages><issn>1347-9032</issn><issn>1349-7006</issn><eissn>1349-7006</eissn><abstract>An elevated serum level of NM23‐H1 protein is found in acute myelogenous leukemia (AML), and predicts a poor treatment outcome in AML patients. To investigate the potential pathological link between the elevated serum level of this protein and poor prognosis, we examined the extracellular effects of recombinant NM23‐H1 protein on the in vitro growth and survival of primary cultured AML cells at concentrations equivalent to the levels found in the serum of AML patients. Extracellular NM23‐H1 protein promoted the in vitro growth and survival of AML cells and this activity was associated with the cytokine production and activation of the MAPK and signal transducers and activators of transcription signaling pathways. Inhibitors specific to MAPK signaling pathways inhibited the growth‐ and survival‐promoting activity of NM23‐H1. These findings indicate the novel biological action of extracellular NM23‐H1 and its association with poor prognosis, and suggest an important role for extracellular NM23‐H1 in the malignant progression of leukemia and a potential therapeutic target for these malignancies. 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| ispartof | Cancer science, 2009-10, Vol.100 (10), p.1885-1894 |
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| source | Wiley Online Library (Open Access Collection) |
| subjects | Biological and medical sciences Biomarkers, Tumor - analysis Blotting, Western Cell Line, Tumor Cell Proliferation Cell Survival - physiology Cytokines - metabolism Extracellular Fluid - chemistry Hematologic and hematopoietic diseases Humans Leukemia, Myeloid, Acute - genetics Leukemia, Myeloid, Acute - metabolism Leukemia, Myeloid, Acute - pathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences NM23 Nucleoside Diphosphate Kinases - genetics NM23 Nucleoside Diphosphate Kinases - metabolism Original Prognosis Recombinant Proteins - genetics Recombinant Proteins - metabolism Signal Transduction - physiology Tumors |
| title | Extracellular NM23 protein promotes the growth and survival of primary cultured human acute myelogenous leukemia cells |
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