miR-29c&b2 encourage extramedullary infiltration resulting in the poor prognosis of acute myeloid leukemia
Extramedullary infiltration (EMI), as a concomitant symptom of acute myeloid leukemia (AML), is associated with low complete remission and poor prognosis in AML. However, the mechanism of EMI remains indistinct. Clinical trials showed that increased miR-29s were associated with a poor overall surviv...
Gespeichert in:
| Veröffentlicht in: | Oncogene 2021-05, Vol.40 (19), p.3434-3448 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 3448 |
|---|---|
| container_issue | 19 |
| container_start_page | 3434 |
| container_title | Oncogene |
| container_volume | 40 |
| creator | Wei, Yanyu Lu, Wei Yu, Yehua Zhai, Yuanmei Guo, Hezhou Yang, Shaoxin Zhao, Chong Zhang, Yanjie Liu, Jiali Liu, Yuhui Fei, Jian Shi, Jun |
| description | Extramedullary infiltration (EMI), as a concomitant symptom of acute myeloid leukemia (AML), is associated with low complete remission and poor prognosis in AML. However, the mechanism of EMI remains indistinct. Clinical trials showed that increased miR-29s were associated with a poor overall survival in AML [
14
]. Nevertheless, they were proved to work as tumor suppressor genes by encouraging apoptosis and inhibiting proliferation in vitro. These contradictory results led us to the hypothesis that miR-29s may play a notable role in the prognosis of AML rather than leukemogenesis. Thus, we explored the specimens of AML patients and addressed this issue into miR-29c&b2 knockout mice. As a result, a poor overall survival and invasive blast cells were observed in high miR-29c&b2-expression patients, and the wildtype mice presented a shorter survival with heavier leukemia infiltration in extramedullary organs. Subsequently, we found that the miR-29c&b2 inside leukemia cells promoted EMI, but not the one in the microenvironment. The analysis of signal pathway revealed that miR-29c&b2 could target HMG-box transcription factor 1 (Hbp1) directly, then reduced Hbp1 bound to the promoter of non-muscle myosin IIB (Myh10) as a transcript inhibitor. Thus, increased Myh10 encouraged the migration of leukemia cells. Accordingly, AML patients with EMI were confirmed to have high miR-29c&b2 and MYH10 with low HBP1. Therefore, we identify that miR-29c&b2 contribute to the poor prognosis of AML patients by promoting EMI, and related genes analyses are prospectively feasible in assessment of AML outcome. |
| doi_str_mv | 10.1038/s41388-021-01775-9 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_2518545911</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A661589751</galeid><sourcerecordid>A661589751</sourcerecordid><originalsourceid>FETCH-LOGICAL-c442t-a3f41dfb76e893668a617297384f24abd2d33200788201f2bb326c995e8562be3</originalsourceid><addsrcrecordid>eNp9UV2L1TAUDKK419U_4IMEBPGla74_HpfFL1gQRJ9D2p7WXNvmmrTg_nvP9a4uikgeAufMDGdmCHnK2QVn0r2qikvnGiZ4w7i1uvH3yI4raxqtvbpPdsxr1nghxRl5VOueMWY9Ew_JmUSec8btyH5OHxvhuxetoLB0eStxBArf1xJn6LdpiuWGpmVIE07WlBdaoG7TmpYRx3T9AvSQc6GHkscl11RpHmjsthXofANTTj2dYPsKc4qPyYMhThWe3P7n5POb15-u3jXXH96-v7q8bjqlxNpEOSjeD6014Lw0xkXDrfBWOjUIFdte9FIKtOKcYHwQbSuF6bzX4LQRLchz8vKkizd926CuYU61A7SyQN5qEJo7rbTnHKHP_4LuMYEFr0OU0JiRdeoONcYJAoaRMYvuKBoujeHaeauPWhf_QOHr0XyXF8AM4U-COBG6kmstMIRDSTPmHTgLx4LDqeCABYefBQePpGe3F28tFvSb8qtRBMgToOJqGaHcWfqP7A-_2a7y</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2525888784</pqid></control><display><type>article</type><title>miR-29c&b2 encourage extramedullary infiltration resulting in the poor prognosis of acute myeloid leukemia</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Wei, Yanyu ; Lu, Wei ; Yu, Yehua ; Zhai, Yuanmei ; Guo, Hezhou ; Yang, Shaoxin ; Zhao, Chong ; Zhang, Yanjie ; Liu, Jiali ; Liu, Yuhui ; Fei, Jian ; Shi, Jun</creator><creatorcontrib>Wei, Yanyu ; Lu, Wei ; Yu, Yehua ; Zhai, Yuanmei ; Guo, Hezhou ; Yang, Shaoxin ; Zhao, Chong ; Zhang, Yanjie ; Liu, Jiali ; Liu, Yuhui ; Fei, Jian ; Shi, Jun</creatorcontrib><description><![CDATA[Extramedullary infiltration (EMI), as a concomitant symptom of acute myeloid leukemia (AML), is associated with low complete remission and poor prognosis in AML. However, the mechanism of EMI remains indistinct. Clinical trials showed that increased miR-29s were associated with a poor overall survival in AML [
14
]. Nevertheless, they were proved to work as tumor suppressor genes by encouraging apoptosis and inhibiting proliferation in vitro. These contradictory results led us to the hypothesis that miR-29s may play a notable role in the prognosis of AML rather than leukemogenesis. Thus, we explored the specimens of AML patients and addressed this issue into miR-29c&b2 knockout mice. As a result, a poor overall survival and invasive blast cells were observed in high miR-29c&b2-expression patients, and the wildtype mice presented a shorter survival with heavier leukemia infiltration in extramedullary organs. Subsequently, we found that the miR-29c&b2 inside leukemia cells promoted EMI, but not the one in the microenvironment. The analysis of signal pathway revealed that miR-29c&b2 could target HMG-box transcription factor 1 (Hbp1) directly, then reduced Hbp1 bound to the promoter of non-muscle myosin IIB (Myh10) as a transcript inhibitor. Thus, increased Myh10 encouraged the migration of leukemia cells. Accordingly, AML patients with EMI were confirmed to have high miR-29c&b2 and MYH10 with low HBP1. Therefore, we identify that miR-29c&b2 contribute to the poor prognosis of AML patients by promoting EMI, and related genes analyses are prospectively feasible in assessment of AML outcome.]]></description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/s41388-021-01775-9</identifier><identifier>PMID: 33888868</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/31 ; 13/51 ; 14/34 ; 14/63 ; 38/91 ; 631/67/1990/283 ; 631/80/84 ; 64/60 ; Acute myeloid leukemia ; Adult ; Aged ; Animals ; Apoptosis ; Blast cells ; Cell Biology ; Cell Line, Tumor ; Cell migration ; Clinical trials ; Computational Biology - methods ; Databases, Genetic ; Disease Models, Animal ; Female ; Health aspects ; High Mobility Group Proteins - metabolism ; Human Genetics ; Humans ; Infiltration ; Internal Medicine ; Invasiveness ; Leukemia ; Leukemia, Myeloid, Acute - genetics ; Leukemia, Myeloid, Acute - metabolism ; Leukemia, Myeloid, Acute - pathology ; Leukemic Infiltration - genetics ; Leukemic Infiltration - metabolism ; Leukemic Infiltration - pathology ; Leukemogenesis ; Male ; Medical prognosis ; Medicine ; Medicine & Public Health ; Metastases ; Mice ; Mice, Knockout ; Microenvironments ; MicroRNA ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Middle Aged ; Myeloid leukemia ; Myosin ; Myosin Heavy Chains - metabolism ; Nonmuscle Myosin Type IIB - metabolism ; Oncology ; Prognosis ; Remission ; Repressor Proteins - metabolism ; Survival Rate ; Tumor suppressor genes ; Young Adult</subject><ispartof>Oncogene, 2021-05, Vol.40 (19), p.3434-3448</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Limited 2021</rights><rights>COPYRIGHT 2021 Nature Publishing Group</rights><rights>The Author(s), under exclusive licence to Springer Nature Limited 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-a3f41dfb76e893668a617297384f24abd2d33200788201f2bb326c995e8562be3</citedby><cites>FETCH-LOGICAL-c442t-a3f41dfb76e893668a617297384f24abd2d33200788201f2bb326c995e8562be3</cites><orcidid>0000-0002-5127-0321 ; 0000-0003-0780-5242 ; 0000-0002-5952-8948 ; 0000-0001-7755-0818</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41388-021-01775-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41388-021-01775-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33888868$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wei, Yanyu</creatorcontrib><creatorcontrib>Lu, Wei</creatorcontrib><creatorcontrib>Yu, Yehua</creatorcontrib><creatorcontrib>Zhai, Yuanmei</creatorcontrib><creatorcontrib>Guo, Hezhou</creatorcontrib><creatorcontrib>Yang, Shaoxin</creatorcontrib><creatorcontrib>Zhao, Chong</creatorcontrib><creatorcontrib>Zhang, Yanjie</creatorcontrib><creatorcontrib>Liu, Jiali</creatorcontrib><creatorcontrib>Liu, Yuhui</creatorcontrib><creatorcontrib>Fei, Jian</creatorcontrib><creatorcontrib>Shi, Jun</creatorcontrib><title>miR-29c&b2 encourage extramedullary infiltration resulting in the poor prognosis of acute myeloid leukemia</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description><![CDATA[Extramedullary infiltration (EMI), as a concomitant symptom of acute myeloid leukemia (AML), is associated with low complete remission and poor prognosis in AML. However, the mechanism of EMI remains indistinct. Clinical trials showed that increased miR-29s were associated with a poor overall survival in AML [
14
]. Nevertheless, they were proved to work as tumor suppressor genes by encouraging apoptosis and inhibiting proliferation in vitro. These contradictory results led us to the hypothesis that miR-29s may play a notable role in the prognosis of AML rather than leukemogenesis. Thus, we explored the specimens of AML patients and addressed this issue into miR-29c&b2 knockout mice. As a result, a poor overall survival and invasive blast cells were observed in high miR-29c&b2-expression patients, and the wildtype mice presented a shorter survival with heavier leukemia infiltration in extramedullary organs. Subsequently, we found that the miR-29c&b2 inside leukemia cells promoted EMI, but not the one in the microenvironment. The analysis of signal pathway revealed that miR-29c&b2 could target HMG-box transcription factor 1 (Hbp1) directly, then reduced Hbp1 bound to the promoter of non-muscle myosin IIB (Myh10) as a transcript inhibitor. Thus, increased Myh10 encouraged the migration of leukemia cells. Accordingly, AML patients with EMI were confirmed to have high miR-29c&b2 and MYH10 with low HBP1. Therefore, we identify that miR-29c&b2 contribute to the poor prognosis of AML patients by promoting EMI, and related genes analyses are prospectively feasible in assessment of AML outcome.]]></description><subject>13/31</subject><subject>13/51</subject><subject>14/34</subject><subject>14/63</subject><subject>38/91</subject><subject>631/67/1990/283</subject><subject>631/80/84</subject><subject>64/60</subject><subject>Acute myeloid leukemia</subject><subject>Adult</subject><subject>Aged</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Blast cells</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Clinical trials</subject><subject>Computational Biology - methods</subject><subject>Databases, Genetic</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Health aspects</subject><subject>High Mobility Group Proteins - metabolism</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Infiltration</subject><subject>Internal Medicine</subject><subject>Invasiveness</subject><subject>Leukemia</subject><subject>Leukemia, Myeloid, Acute - genetics</subject><subject>Leukemia, Myeloid, Acute - metabolism</subject><subject>Leukemia, Myeloid, Acute - pathology</subject><subject>Leukemic Infiltration - genetics</subject><subject>Leukemic Infiltration - metabolism</subject><subject>Leukemic Infiltration - pathology</subject><subject>Leukemogenesis</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastases</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Microenvironments</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Middle Aged</subject><subject>Myeloid leukemia</subject><subject>Myosin</subject><subject>Myosin Heavy Chains - metabolism</subject><subject>Nonmuscle Myosin Type IIB - metabolism</subject><subject>Oncology</subject><subject>Prognosis</subject><subject>Remission</subject><subject>Repressor Proteins - metabolism</subject><subject>Survival Rate</subject><subject>Tumor suppressor genes</subject><subject>Young Adult</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9UV2L1TAUDKK419U_4IMEBPGla74_HpfFL1gQRJ9D2p7WXNvmmrTg_nvP9a4uikgeAufMDGdmCHnK2QVn0r2qikvnGiZ4w7i1uvH3yI4raxqtvbpPdsxr1nghxRl5VOueMWY9Ew_JmUSec8btyH5OHxvhuxetoLB0eStxBArf1xJn6LdpiuWGpmVIE07WlBdaoG7TmpYRx3T9AvSQc6GHkscl11RpHmjsthXofANTTj2dYPsKc4qPyYMhThWe3P7n5POb15-u3jXXH96-v7q8bjqlxNpEOSjeD6014Lw0xkXDrfBWOjUIFdte9FIKtOKcYHwQbSuF6bzX4LQRLchz8vKkizd926CuYU61A7SyQN5qEJo7rbTnHKHP_4LuMYEFr0OU0JiRdeoONcYJAoaRMYvuKBoujeHaeauPWhf_QOHr0XyXF8AM4U-COBG6kmstMIRDSTPmHTgLx4LDqeCABYefBQePpGe3F28tFvSb8qtRBMgToOJqGaHcWfqP7A-_2a7y</recordid><startdate>20210513</startdate><enddate>20210513</enddate><creator>Wei, Yanyu</creator><creator>Lu, Wei</creator><creator>Yu, Yehua</creator><creator>Zhai, Yuanmei</creator><creator>Guo, Hezhou</creator><creator>Yang, Shaoxin</creator><creator>Zhao, Chong</creator><creator>Zhang, Yanjie</creator><creator>Liu, Jiali</creator><creator>Liu, Yuhui</creator><creator>Fei, Jian</creator><creator>Shi, Jun</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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-5127-0321</orcidid><orcidid>https://orcid.org/0000-0003-0780-5242</orcidid><orcidid>https://orcid.org/0000-0002-5952-8948</orcidid><orcidid>https://orcid.org/0000-0001-7755-0818</orcidid></search><sort><creationdate>20210513</creationdate><title>miR-29c&b2 encourage extramedullary infiltration resulting in the poor prognosis of acute myeloid leukemia</title><author>Wei, Yanyu ; Lu, Wei ; Yu, Yehua ; Zhai, Yuanmei ; Guo, Hezhou ; Yang, Shaoxin ; Zhao, Chong ; Zhang, Yanjie ; Liu, Jiali ; Liu, Yuhui ; Fei, Jian ; Shi, Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-a3f41dfb76e893668a617297384f24abd2d33200788201f2bb326c995e8562be3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>13/31</topic><topic>13/51</topic><topic>14/34</topic><topic>14/63</topic><topic>38/91</topic><topic>631/67/1990/283</topic><topic>631/80/84</topic><topic>64/60</topic><topic>Acute myeloid leukemia</topic><topic>Adult</topic><topic>Aged</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Blast cells</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Clinical trials</topic><topic>Computational Biology - methods</topic><topic>Databases, Genetic</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Health aspects</topic><topic>High Mobility Group Proteins - metabolism</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Infiltration</topic><topic>Internal Medicine</topic><topic>Invasiveness</topic><topic>Leukemia</topic><topic>Leukemia, Myeloid, Acute - genetics</topic><topic>Leukemia, Myeloid, Acute - metabolism</topic><topic>Leukemia, Myeloid, Acute - pathology</topic><topic>Leukemic Infiltration - genetics</topic><topic>Leukemic Infiltration - metabolism</topic><topic>Leukemic Infiltration - pathology</topic><topic>Leukemogenesis</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metastases</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Microenvironments</topic><topic>MicroRNA</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Middle Aged</topic><topic>Myeloid leukemia</topic><topic>Myosin</topic><topic>Myosin Heavy Chains - metabolism</topic><topic>Nonmuscle Myosin Type IIB - metabolism</topic><topic>Oncology</topic><topic>Prognosis</topic><topic>Remission</topic><topic>Repressor Proteins - metabolism</topic><topic>Survival Rate</topic><topic>Tumor suppressor genes</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wei, Yanyu</creatorcontrib><creatorcontrib>Lu, Wei</creatorcontrib><creatorcontrib>Yu, Yehua</creatorcontrib><creatorcontrib>Zhai, Yuanmei</creatorcontrib><creatorcontrib>Guo, Hezhou</creatorcontrib><creatorcontrib>Yang, Shaoxin</creatorcontrib><creatorcontrib>Zhao, Chong</creatorcontrib><creatorcontrib>Zhang, Yanjie</creatorcontrib><creatorcontrib>Liu, Jiali</creatorcontrib><creatorcontrib>Liu, Yuhui</creatorcontrib><creatorcontrib>Fei, Jian</creatorcontrib><creatorcontrib>Shi, Jun</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>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wei, Yanyu</au><au>Lu, Wei</au><au>Yu, Yehua</au><au>Zhai, Yuanmei</au><au>Guo, Hezhou</au><au>Yang, Shaoxin</au><au>Zhao, Chong</au><au>Zhang, Yanjie</au><au>Liu, Jiali</au><au>Liu, Yuhui</au><au>Fei, Jian</au><au>Shi, Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-29c&b2 encourage extramedullary infiltration resulting in the poor prognosis of acute myeloid leukemia</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2021-05-13</date><risdate>2021</risdate><volume>40</volume><issue>19</issue><spage>3434</spage><epage>3448</epage><pages>3434-3448</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract><![CDATA[Extramedullary infiltration (EMI), as a concomitant symptom of acute myeloid leukemia (AML), is associated with low complete remission and poor prognosis in AML. However, the mechanism of EMI remains indistinct. Clinical trials showed that increased miR-29s were associated with a poor overall survival in AML [
14
]. Nevertheless, they were proved to work as tumor suppressor genes by encouraging apoptosis and inhibiting proliferation in vitro. These contradictory results led us to the hypothesis that miR-29s may play a notable role in the prognosis of AML rather than leukemogenesis. Thus, we explored the specimens of AML patients and addressed this issue into miR-29c&b2 knockout mice. As a result, a poor overall survival and invasive blast cells were observed in high miR-29c&b2-expression patients, and the wildtype mice presented a shorter survival with heavier leukemia infiltration in extramedullary organs. Subsequently, we found that the miR-29c&b2 inside leukemia cells promoted EMI, but not the one in the microenvironment. The analysis of signal pathway revealed that miR-29c&b2 could target HMG-box transcription factor 1 (Hbp1) directly, then reduced Hbp1 bound to the promoter of non-muscle myosin IIB (Myh10) as a transcript inhibitor. Thus, increased Myh10 encouraged the migration of leukemia cells. Accordingly, AML patients with EMI were confirmed to have high miR-29c&b2 and MYH10 with low HBP1. Therefore, we identify that miR-29c&b2 contribute to the poor prognosis of AML patients by promoting EMI, and related genes analyses are prospectively feasible in assessment of AML outcome.]]></abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>33888868</pmid><doi>10.1038/s41388-021-01775-9</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-5127-0321</orcidid><orcidid>https://orcid.org/0000-0003-0780-5242</orcidid><orcidid>https://orcid.org/0000-0002-5952-8948</orcidid><orcidid>https://orcid.org/0000-0001-7755-0818</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0950-9232 |
| ispartof | Oncogene, 2021-05, Vol.40 (19), p.3434-3448 |
| issn | 0950-9232 1476-5594 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2518545911 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | 13/31 13/51 14/34 14/63 38/91 631/67/1990/283 631/80/84 64/60 Acute myeloid leukemia Adult Aged Animals Apoptosis Blast cells Cell Biology Cell Line, Tumor Cell migration Clinical trials Computational Biology - methods Databases, Genetic Disease Models, Animal Female Health aspects High Mobility Group Proteins - metabolism Human Genetics Humans Infiltration Internal Medicine Invasiveness Leukemia Leukemia, Myeloid, Acute - genetics Leukemia, Myeloid, Acute - metabolism Leukemia, Myeloid, Acute - pathology Leukemic Infiltration - genetics Leukemic Infiltration - metabolism Leukemic Infiltration - pathology Leukemogenesis Male Medical prognosis Medicine Medicine & Public Health Metastases Mice Mice, Knockout Microenvironments MicroRNA MicroRNAs - genetics MicroRNAs - metabolism Middle Aged Myeloid leukemia Myosin Myosin Heavy Chains - metabolism Nonmuscle Myosin Type IIB - metabolism Oncology Prognosis Remission Repressor Proteins - metabolism Survival Rate Tumor suppressor genes Young Adult |
| title | miR-29c&b2 encourage extramedullary infiltration resulting in the poor prognosis of acute myeloid leukemia |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T13%3A13%3A10IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=miR-29c&b2%20encourage%20extramedullary%20infiltration%20resulting%20in%20the%20poor%20prognosis%20of%20acute%20myeloid%20leukemia&rft.jtitle=Oncogene&rft.au=Wei,%20Yanyu&rft.date=2021-05-13&rft.volume=40&rft.issue=19&rft.spage=3434&rft.epage=3448&rft.pages=3434-3448&rft.issn=0950-9232&rft.eissn=1476-5594&rft_id=info:doi/10.1038/s41388-021-01775-9&rft_dat=%3Cgale_proqu%3EA661589751%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2525888784&rft_id=info:pmid/33888868&rft_galeid=A661589751&rfr_iscdi=true |