HNF4A-AS1-encoded small peptide promotes self-renewal and aggressiveness of neuroblastoma stem cells via eEF1A1-repressed SMAD4 transactivation
Cancer stem cells play crucial roles in tumorigenesis and aggressiveness, while regulatory mechanisms in neuroblastoma (NB), a pediatric extracranial malignancy with highest incidence, are still unknown. Herein, a small 51-amino acid peptide (sPEP1) encoded by hepatocyte nuclear factor 4 alpha antis...
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| Veröffentlicht in: | Oncogene 2022-04, Vol.41 (17), p.2505-2519 |
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| creator | Song, Huajie Wang, Jianqun Wang, Xiaojing Yuan, Boling Li, Dan Hu, Anpei Guo, Yanhua Cai, Shuang Jin, Shikai Zhou, Yi Li, Qilan Chen, Guo Gao, Haiyang Zheng, Liduan Tong, Qiangsong |
| description | Cancer stem cells play crucial roles in tumorigenesis and aggressiveness, while regulatory mechanisms in neuroblastoma (NB), a pediatric extracranial malignancy with highest incidence, are still unknown. Herein, a small 51-amino acid peptide (sPEP1) encoded by hepatocyte nuclear factor 4 alpha antisense RNA 1 (
HNF4A-AS1
) was identified in tumor tissues and cells, which facilitated self-renewal and aggressiveness of NB stem cells. MiRNA-409-5p interacted with
HNF4A-AS1
to facilitate sPEP1 translation via recruiting eukaryotic translation initiation factor 3 subunit G, while sPEP1 repressed serum deprivation-induced senescence and promoted sphere formation, growth, or metastasis of NB stem cells. Mechanistically, sPEP1 directly interacted with eukaryotic translation elongation factor 1 alpha 1 (eEF1A1) to facilitate its binding to SMAD family member 4 (SMAD4), resulting in repression of SMAD4 transactivation and transcriptional upregulation of stem cell genes associated with tumor progression. Rescue experiments revealed that sPEP1 exerted oncogenic roles via facilitating physical interaction between eEF1A1 and SMAD4. Notably, knockdown of
sPEP1
significantly repressed the self-renewal and metastasis of NB stem cells in vivo. High
sPEP1
or
eEF1A1
levels in clinical NB tissues were linked to poor patients’ survival. These findings suggest that
HNF4A-AS1
-encoded sPEP1 promotes self-renewal and aggressive features of NB stem cells by eEF1A1-repressed SMAD4 transactivation. |
| doi_str_mv | 10.1038/s41388-022-02271-4 |
| format | Article |
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HNF4A-AS1
) was identified in tumor tissues and cells, which facilitated self-renewal and aggressiveness of NB stem cells. MiRNA-409-5p interacted with
HNF4A-AS1
to facilitate sPEP1 translation via recruiting eukaryotic translation initiation factor 3 subunit G, while sPEP1 repressed serum deprivation-induced senescence and promoted sphere formation, growth, or metastasis of NB stem cells. Mechanistically, sPEP1 directly interacted with eukaryotic translation elongation factor 1 alpha 1 (eEF1A1) to facilitate its binding to SMAD family member 4 (SMAD4), resulting in repression of SMAD4 transactivation and transcriptional upregulation of stem cell genes associated with tumor progression. Rescue experiments revealed that sPEP1 exerted oncogenic roles via facilitating physical interaction between eEF1A1 and SMAD4. Notably, knockdown of
sPEP1
significantly repressed the self-renewal and metastasis of NB stem cells in vivo. High
sPEP1
or
eEF1A1
levels in clinical NB tissues were linked to poor patients’ survival. These findings suggest that
HNF4A-AS1
-encoded sPEP1 promotes self-renewal and aggressive features of NB stem cells by eEF1A1-repressed SMAD4 transactivation.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/s41388-022-02271-4</identifier><identifier>PMID: 35318442</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/109 ; 13/31 ; 13/51 ; 13/89 ; 14/19 ; 38/39 ; 38/77 ; 631/67/2332 ; 631/67/395 ; 64/60 ; Antisense RNA ; Apoptosis ; Carcinogenesis - genetics ; Cell Biology ; Cell Line, Tumor ; Cell self-renewal ; Child ; Gene Expression Regulation, Neoplastic ; Hepatocyte nuclear factor 4 ; Hepatocyte Nuclear Factor 4 - genetics ; Hepatocyte Nuclear Factor 4 - metabolism ; Human Genetics ; Humans ; Internal Medicine ; Malignancy ; Medicine ; Medicine & Public Health ; Metastases ; Metastasis ; MicroRNAs - genetics ; miRNA ; Neuroblastoma ; Neuroblastoma - pathology ; Oncology ; Pediatrics ; Peptide Elongation Factor 1 - genetics ; Peptide Elongation Factor 1 - metabolism ; Peptides ; RNA, Antisense ; RNA, Long Noncoding - genetics ; Senescence ; Smad protein ; Smad4 protein ; Smad4 Protein - genetics ; Smad4 Protein - metabolism ; Stem cells ; Stem Cells - metabolism ; Transcription ; Transcriptional Activation ; Translation ; Translation elongation ; Tumorigenesis</subject><ispartof>Oncogene, 2022-04, Vol.41 (17), p.2505-2519</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Limited 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer Nature Limited.</rights><rights>The Author(s), under exclusive licence to Springer Nature Limited 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-b2b8e0424d686c60ae28af120922563fb6680b3d5b2a8f45d9f9e3ed06d26c4f3</citedby><cites>FETCH-LOGICAL-c375t-b2b8e0424d686c60ae28af120922563fb6680b3d5b2a8f45d9f9e3ed06d26c4f3</cites><orcidid>0000-0002-2615-6404 ; 0000-0001-5566-673X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35318442$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Song, Huajie</creatorcontrib><creatorcontrib>Wang, Jianqun</creatorcontrib><creatorcontrib>Wang, Xiaojing</creatorcontrib><creatorcontrib>Yuan, Boling</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Hu, Anpei</creatorcontrib><creatorcontrib>Guo, Yanhua</creatorcontrib><creatorcontrib>Cai, Shuang</creatorcontrib><creatorcontrib>Jin, Shikai</creatorcontrib><creatorcontrib>Zhou, Yi</creatorcontrib><creatorcontrib>Li, Qilan</creatorcontrib><creatorcontrib>Chen, Guo</creatorcontrib><creatorcontrib>Gao, Haiyang</creatorcontrib><creatorcontrib>Zheng, Liduan</creatorcontrib><creatorcontrib>Tong, Qiangsong</creatorcontrib><title>HNF4A-AS1-encoded small peptide promotes self-renewal and aggressiveness of neuroblastoma stem cells via eEF1A1-repressed SMAD4 transactivation</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Cancer stem cells play crucial roles in tumorigenesis and aggressiveness, while regulatory mechanisms in neuroblastoma (NB), a pediatric extracranial malignancy with highest incidence, are still unknown. Herein, a small 51-amino acid peptide (sPEP1) encoded by hepatocyte nuclear factor 4 alpha antisense RNA 1 (
HNF4A-AS1
) was identified in tumor tissues and cells, which facilitated self-renewal and aggressiveness of NB stem cells. MiRNA-409-5p interacted with
HNF4A-AS1
to facilitate sPEP1 translation via recruiting eukaryotic translation initiation factor 3 subunit G, while sPEP1 repressed serum deprivation-induced senescence and promoted sphere formation, growth, or metastasis of NB stem cells. Mechanistically, sPEP1 directly interacted with eukaryotic translation elongation factor 1 alpha 1 (eEF1A1) to facilitate its binding to SMAD family member 4 (SMAD4), resulting in repression of SMAD4 transactivation and transcriptional upregulation of stem cell genes associated with tumor progression. Rescue experiments revealed that sPEP1 exerted oncogenic roles via facilitating physical interaction between eEF1A1 and SMAD4. Notably, knockdown of
sPEP1
significantly repressed the self-renewal and metastasis of NB stem cells in vivo. High
sPEP1
or
eEF1A1
levels in clinical NB tissues were linked to poor patients’ survival. These findings suggest that
HNF4A-AS1
-encoded sPEP1 promotes self-renewal and aggressive features of NB stem cells by eEF1A1-repressed SMAD4 transactivation.</description><subject>13/1</subject><subject>13/109</subject><subject>13/31</subject><subject>13/51</subject><subject>13/89</subject><subject>14/19</subject><subject>38/39</subject><subject>38/77</subject><subject>631/67/2332</subject><subject>631/67/395</subject><subject>64/60</subject><subject>Antisense RNA</subject><subject>Apoptosis</subject><subject>Carcinogenesis - genetics</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell self-renewal</subject><subject>Child</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Hepatocyte nuclear factor 4</subject><subject>Hepatocyte Nuclear Factor 4 - genetics</subject><subject>Hepatocyte Nuclear Factor 4 - metabolism</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Malignancy</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>Neuroblastoma</subject><subject>Neuroblastoma - pathology</subject><subject>Oncology</subject><subject>Pediatrics</subject><subject>Peptide Elongation Factor 1 - genetics</subject><subject>Peptide Elongation Factor 1 - metabolism</subject><subject>Peptides</subject><subject>RNA, Antisense</subject><subject>RNA, Long Noncoding - genetics</subject><subject>Senescence</subject><subject>Smad protein</subject><subject>Smad4 protein</subject><subject>Smad4 Protein - genetics</subject><subject>Smad4 Protein - metabolism</subject><subject>Stem cells</subject><subject>Stem Cells - metabolism</subject><subject>Transcription</subject><subject>Transcriptional Activation</subject><subject>Translation</subject><subject>Translation elongation</subject><subject>Tumorigenesis</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9UcluFDEQtRCIDIEf4IAscTZ4H_exFTIEKcAhcLbc7fKoo95weQbxFfwyHibAjUPJUvktqvcIeSn4G8GVe4taKOcYl_I0W8H0I7IRemuZMY1-TDa8MZw1UskL8gzxnnO-bbh8Si6UUcJpLTfk582nnW5ZeycYzP0SIVKcwjjSFdYyRKBrXqalAFKEMbEMM3wPIw1zpGG_z4A4HOsOkS6JznDISzcGLMsUKBaYaA_jiPQ4BArXO9GKqrCeWNXn7mP7TtOSw4yhL8MxlGGZn5MnKYwILx7eS_J1d_3l6obdfn7_4aq9Zb3amsI62TngWupone0tDyBdSELyRkpjVeqsdbxT0XQyuKRNbFIDCiK3UdpeJ3VJXp91633fDoDF3y-HPFdLL61RNVnb8IqSZ1SfF8QMya95mEL-4QX3pw78uQNf8_e_O_C6kl49SB-6CeJfyp_QK0CdAVi_5j3kf97_kf0FCT2Stw</recordid><startdate>20220422</startdate><enddate>20220422</enddate><creator>Song, Huajie</creator><creator>Wang, Jianqun</creator><creator>Wang, Xiaojing</creator><creator>Yuan, Boling</creator><creator>Li, Dan</creator><creator>Hu, Anpei</creator><creator>Guo, Yanhua</creator><creator>Cai, Shuang</creator><creator>Jin, Shikai</creator><creator>Zhou, Yi</creator><creator>Li, Qilan</creator><creator>Chen, Guo</creator><creator>Gao, Haiyang</creator><creator>Zheng, Liduan</creator><creator>Tong, Qiangsong</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><orcidid>https://orcid.org/0000-0002-2615-6404</orcidid><orcidid>https://orcid.org/0000-0001-5566-673X</orcidid></search><sort><creationdate>20220422</creationdate><title>HNF4A-AS1-encoded small peptide promotes self-renewal and aggressiveness of neuroblastoma stem cells via eEF1A1-repressed SMAD4 transactivation</title><author>Song, Huajie ; Wang, Jianqun ; Wang, Xiaojing ; Yuan, Boling ; Li, Dan ; Hu, Anpei ; Guo, Yanhua ; Cai, Shuang ; Jin, Shikai ; Zhou, Yi ; Li, Qilan ; Chen, Guo ; Gao, Haiyang ; Zheng, Liduan ; Tong, Qiangsong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-b2b8e0424d686c60ae28af120922563fb6680b3d5b2a8f45d9f9e3ed06d26c4f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>13/1</topic><topic>13/109</topic><topic>13/31</topic><topic>13/51</topic><topic>13/89</topic><topic>14/19</topic><topic>38/39</topic><topic>38/77</topic><topic>631/67/2332</topic><topic>631/67/395</topic><topic>64/60</topic><topic>Antisense RNA</topic><topic>Apoptosis</topic><topic>Carcinogenesis - genetics</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell self-renewal</topic><topic>Child</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Hepatocyte nuclear factor 4</topic><topic>Hepatocyte Nuclear Factor 4 - genetics</topic><topic>Hepatocyte Nuclear Factor 4 - metabolism</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Malignancy</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>Neuroblastoma</topic><topic>Neuroblastoma - pathology</topic><topic>Oncology</topic><topic>Pediatrics</topic><topic>Peptide Elongation Factor 1 - genetics</topic><topic>Peptide Elongation Factor 1 - metabolism</topic><topic>Peptides</topic><topic>RNA, Antisense</topic><topic>RNA, Long Noncoding - genetics</topic><topic>Senescence</topic><topic>Smad protein</topic><topic>Smad4 protein</topic><topic>Smad4 Protein - genetics</topic><topic>Smad4 Protein - metabolism</topic><topic>Stem cells</topic><topic>Stem Cells - metabolism</topic><topic>Transcription</topic><topic>Transcriptional Activation</topic><topic>Translation</topic><topic>Translation elongation</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Song, Huajie</creatorcontrib><creatorcontrib>Wang, Jianqun</creatorcontrib><creatorcontrib>Wang, Xiaojing</creatorcontrib><creatorcontrib>Yuan, Boling</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Hu, Anpei</creatorcontrib><creatorcontrib>Guo, Yanhua</creatorcontrib><creatorcontrib>Cai, Shuang</creatorcontrib><creatorcontrib>Jin, Shikai</creatorcontrib><creatorcontrib>Zhou, Yi</creatorcontrib><creatorcontrib>Li, Qilan</creatorcontrib><creatorcontrib>Chen, Guo</creatorcontrib><creatorcontrib>Gao, Haiyang</creatorcontrib><creatorcontrib>Zheng, Liduan</creatorcontrib><creatorcontrib>Tong, Qiangsong</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><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Song, Huajie</au><au>Wang, Jianqun</au><au>Wang, Xiaojing</au><au>Yuan, Boling</au><au>Li, Dan</au><au>Hu, Anpei</au><au>Guo, Yanhua</au><au>Cai, Shuang</au><au>Jin, Shikai</au><au>Zhou, Yi</au><au>Li, Qilan</au><au>Chen, Guo</au><au>Gao, Haiyang</au><au>Zheng, Liduan</au><au>Tong, Qiangsong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HNF4A-AS1-encoded small peptide promotes self-renewal and aggressiveness of neuroblastoma stem cells via eEF1A1-repressed SMAD4 transactivation</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2022-04-22</date><risdate>2022</risdate><volume>41</volume><issue>17</issue><spage>2505</spage><epage>2519</epage><pages>2505-2519</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>Cancer stem cells play crucial roles in tumorigenesis and aggressiveness, while regulatory mechanisms in neuroblastoma (NB), a pediatric extracranial malignancy with highest incidence, are still unknown. Herein, a small 51-amino acid peptide (sPEP1) encoded by hepatocyte nuclear factor 4 alpha antisense RNA 1 (
HNF4A-AS1
) was identified in tumor tissues and cells, which facilitated self-renewal and aggressiveness of NB stem cells. MiRNA-409-5p interacted with
HNF4A-AS1
to facilitate sPEP1 translation via recruiting eukaryotic translation initiation factor 3 subunit G, while sPEP1 repressed serum deprivation-induced senescence and promoted sphere formation, growth, or metastasis of NB stem cells. Mechanistically, sPEP1 directly interacted with eukaryotic translation elongation factor 1 alpha 1 (eEF1A1) to facilitate its binding to SMAD family member 4 (SMAD4), resulting in repression of SMAD4 transactivation and transcriptional upregulation of stem cell genes associated with tumor progression. Rescue experiments revealed that sPEP1 exerted oncogenic roles via facilitating physical interaction between eEF1A1 and SMAD4. Notably, knockdown of
sPEP1
significantly repressed the self-renewal and metastasis of NB stem cells in vivo. High
sPEP1
or
eEF1A1
levels in clinical NB tissues were linked to poor patients’ survival. These findings suggest that
HNF4A-AS1
-encoded sPEP1 promotes self-renewal and aggressive features of NB stem cells by eEF1A1-repressed SMAD4 transactivation.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>35318442</pmid><doi>10.1038/s41388-022-02271-4</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-2615-6404</orcidid><orcidid>https://orcid.org/0000-0001-5566-673X</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0950-9232 |
| ispartof | Oncogene, 2022-04, Vol.41 (17), p.2505-2519 |
| issn | 0950-9232 1476-5594 |
| language | eng |
| recordid | cdi_proquest_journals_2653413690 |
| source | MEDLINE; Alma/SFX Local Collection |
| subjects | 13/1 13/109 13/31 13/51 13/89 14/19 38/39 38/77 631/67/2332 631/67/395 64/60 Antisense RNA Apoptosis Carcinogenesis - genetics Cell Biology Cell Line, Tumor Cell self-renewal Child Gene Expression Regulation, Neoplastic Hepatocyte nuclear factor 4 Hepatocyte Nuclear Factor 4 - genetics Hepatocyte Nuclear Factor 4 - metabolism Human Genetics Humans Internal Medicine Malignancy Medicine Medicine & Public Health Metastases Metastasis MicroRNAs - genetics miRNA Neuroblastoma Neuroblastoma - pathology Oncology Pediatrics Peptide Elongation Factor 1 - genetics Peptide Elongation Factor 1 - metabolism Peptides RNA, Antisense RNA, Long Noncoding - genetics Senescence Smad protein Smad4 protein Smad4 Protein - genetics Smad4 Protein - metabolism Stem cells Stem Cells - metabolism Transcription Transcriptional Activation Translation Translation elongation Tumorigenesis |
| title | HNF4A-AS1-encoded small peptide promotes self-renewal and aggressiveness of neuroblastoma stem cells via eEF1A1-repressed SMAD4 transactivation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-24T22%3A39%3A40IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=HNF4A-AS1-encoded%20small%20peptide%20promotes%20self-renewal%20and%20aggressiveness%20of%20neuroblastoma%20stem%20cells%20via%20eEF1A1-repressed%20SMAD4%20transactivation&rft.jtitle=Oncogene&rft.au=Song,%20Huajie&rft.date=2022-04-22&rft.volume=41&rft.issue=17&rft.spage=2505&rft.epage=2519&rft.pages=2505-2519&rft.issn=0950-9232&rft.eissn=1476-5594&rft_id=info:doi/10.1038/s41388-022-02271-4&rft_dat=%3Cproquest_cross%3E2653413690%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2653413690&rft_id=info:pmid/35318442&rfr_iscdi=true |