Pro-Angiogenic Role of LncRNA HULC in Microvascular Endothelial Cells via Sequestrating miR-124
HULC is a multifunctional lncRNA that has pro-angiogenic function in various cancers. The present study was designed to see the role of lncRNA HULC in normal endothelial cells angiogenesis. Cell viability, apoptosis, migration, tube formation and expression levels of angiogenesis-related proteins we...
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| Veröffentlicht in: | Cellular physiology and biochemistry 2018-01, Vol.50 (6), p.2188-2202 |
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| creator | Yin, Dexin Li, Yezhou Fu, Changgeng Feng, Ye |
| description | HULC is a multifunctional lncRNA that has pro-angiogenic function in various cancers. The present study was designed to see the role of lncRNA HULC in normal endothelial cells angiogenesis.
Cell viability, apoptosis, migration, tube formation and expression levels of angiogenesis-related proteins were respectively assessed in human microvascular endothelial HMEC-1 cells after lncRNA HULC was silenced by shRNA transfection. Cross-regulation between lncRNA HULC and miR-124, and between miR-124 and MCL-1 were detected by qRT-PCR, sequence analysis, and luciferase reporter assay.
Silence of lncRNA HULC significantly reduced viability, migration, tube formation and protein levels of VEGF, VEGFR2, CD144 and eNOS in HMEC-1 cells. Meanwhile, silence of lncRNA HULC induced apoptosis in HMEC-1 cells, as Bcl-2 was down-regulated, Bax was up-regulated, and caspase-3 and -9 were cleaved. miR-124 expression was negatively regulated by lncRNA HULC, and HULC worked as a molecular sponge for miR-124, in having miR-124 exhausted. Besides, MCL-1 was a target gene of miR-124. Rescue assay results showed that the effects of lncRNA HULC silence on HMEC-1 cells growth, migration and angiogenesis were abolished by miR-124 suppression. Similarly, the effects of miR-124 on HMEC-1 cells were abolished by MCL-1 overexpression. Furthermore, MCL-1 activated PI3K/AKT and JAK/STAT signaling pathways.
These findings suggest a pro-angiogenic role of lncRNA HULC in endothelial cells. The pro-angiogenic actions of lncRNA HULC may be through sponging miR-124, preventing MCL-1 from degradation by miR-124. |
| doi_str_mv | 10.1159/000495060 |
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Cell viability, apoptosis, migration, tube formation and expression levels of angiogenesis-related proteins were respectively assessed in human microvascular endothelial HMEC-1 cells after lncRNA HULC was silenced by shRNA transfection. Cross-regulation between lncRNA HULC and miR-124, and between miR-124 and MCL-1 were detected by qRT-PCR, sequence analysis, and luciferase reporter assay.
Silence of lncRNA HULC significantly reduced viability, migration, tube formation and protein levels of VEGF, VEGFR2, CD144 and eNOS in HMEC-1 cells. Meanwhile, silence of lncRNA HULC induced apoptosis in HMEC-1 cells, as Bcl-2 was down-regulated, Bax was up-regulated, and caspase-3 and -9 were cleaved. miR-124 expression was negatively regulated by lncRNA HULC, and HULC worked as a molecular sponge for miR-124, in having miR-124 exhausted. Besides, MCL-1 was a target gene of miR-124. Rescue assay results showed that the effects of lncRNA HULC silence on HMEC-1 cells growth, migration and angiogenesis were abolished by miR-124 suppression. Similarly, the effects of miR-124 on HMEC-1 cells were abolished by MCL-1 overexpression. Furthermore, MCL-1 activated PI3K/AKT and JAK/STAT signaling pathways.
These findings suggest a pro-angiogenic role of lncRNA HULC in endothelial cells. The pro-angiogenic actions of lncRNA HULC may be through sponging miR-124, preventing MCL-1 from degradation by miR-124.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000495060</identifier><identifier>PMID: 30415256</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Angiogenesis ; Antagomirs - metabolism ; Atherosclerosis ; bcl-2-Associated X Protein - metabolism ; Caspase 3 - metabolism ; Cell Line ; Cell Movement ; Cell Survival ; DNA methylation ; Endothelial Cells - cytology ; Endothelial Cells - metabolism ; HMEC-1 cell ; Humans ; Kinases ; Liver cancer ; LncRNA HULC ; MCL-1 ; MicroRNAs ; MicroRNAs - antagonists & inhibitors ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miR-124 ; Myeloid Cell Leukemia Sequence 1 Protein - chemistry ; Myeloid Cell Leukemia Sequence 1 Protein - genetics ; Myeloid Cell Leukemia Sequence 1 Protein - metabolism ; Neovascularization, Physiologic ; Nitric oxide ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Retracted Paper ; RNA Interference ; RNA, Long Noncoding - antagonists & inhibitors ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; RNA, Small Interfering - metabolism ; Signal Transduction ; STAT3 Transcription Factor - metabolism ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>Cellular physiology and biochemistry, 2018-01, Vol.50 (6), p.2188-2202</ispartof><rights>2018 The Author(s). Published by S. Karger AG, Basel</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-d299a0ce51a041a276e5cf31680cfaa92e69388e4a602fa8cfb790d27c37f6f83</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,2096,27612,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30415256$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yin, Dexin</creatorcontrib><creatorcontrib>Li, Yezhou</creatorcontrib><creatorcontrib>Fu, Changgeng</creatorcontrib><creatorcontrib>Feng, Ye</creatorcontrib><title>Pro-Angiogenic Role of LncRNA HULC in Microvascular Endothelial Cells via Sequestrating miR-124</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>HULC is a multifunctional lncRNA that has pro-angiogenic function in various cancers. The present study was designed to see the role of lncRNA HULC in normal endothelial cells angiogenesis.
Cell viability, apoptosis, migration, tube formation and expression levels of angiogenesis-related proteins were respectively assessed in human microvascular endothelial HMEC-1 cells after lncRNA HULC was silenced by shRNA transfection. Cross-regulation between lncRNA HULC and miR-124, and between miR-124 and MCL-1 were detected by qRT-PCR, sequence analysis, and luciferase reporter assay.
Silence of lncRNA HULC significantly reduced viability, migration, tube formation and protein levels of VEGF, VEGFR2, CD144 and eNOS in HMEC-1 cells. Meanwhile, silence of lncRNA HULC induced apoptosis in HMEC-1 cells, as Bcl-2 was down-regulated, Bax was up-regulated, and caspase-3 and -9 were cleaved. miR-124 expression was negatively regulated by lncRNA HULC, and HULC worked as a molecular sponge for miR-124, in having miR-124 exhausted. Besides, MCL-1 was a target gene of miR-124. Rescue assay results showed that the effects of lncRNA HULC silence on HMEC-1 cells growth, migration and angiogenesis were abolished by miR-124 suppression. Similarly, the effects of miR-124 on HMEC-1 cells were abolished by MCL-1 overexpression. Furthermore, MCL-1 activated PI3K/AKT and JAK/STAT signaling pathways.
These findings suggest a pro-angiogenic role of lncRNA HULC in endothelial cells. The pro-angiogenic actions of lncRNA HULC may be through sponging miR-124, preventing MCL-1 from degradation by miR-124.</description><subject>Angiogenesis</subject><subject>Antagomirs - metabolism</subject><subject>Atherosclerosis</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Line</subject><subject>Cell Movement</subject><subject>Cell Survival</subject><subject>DNA methylation</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - metabolism</subject><subject>HMEC-1 cell</subject><subject>Humans</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>LncRNA HULC</subject><subject>MCL-1</subject><subject>MicroRNAs</subject><subject>MicroRNAs - antagonists & inhibitors</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miR-124</subject><subject>Myeloid Cell Leukemia Sequence 1 Protein - chemistry</subject><subject>Myeloid Cell Leukemia Sequence 1 Protein - genetics</subject><subject>Myeloid Cell Leukemia Sequence 1 Protein - metabolism</subject><subject>Neovascularization, Physiologic</subject><subject>Nitric oxide</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Retracted Paper</subject><subject>RNA Interference</subject><subject>RNA, Long Noncoding - antagonists & inhibitors</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Signal Transduction</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptkUtv1DAUhSMEoqWwYI-QJTawSPEjju3lELW00hSqga6tG8cOHjLx1E4q9d_XdIaphFj5oc_nnuNTFG8JPiWEq88Y40pxXONnxTGpKCmVEPJ53mPCS6mkOCpepbTG-SgUfVkcMVwRTnl9XOjrGMrF2PvQ29EbtAqDRcGh5WhW3xbo4mbZID-iK29iuINk5gEiOhu7MP2yg4cBNXYYErrzgH7Y29mmKcLkxx5t_KoktHpdvHAwJPtmv54UN-dnP5uLcvn962WzWJamqtlUdlQpwMZyAtkaUFFbbhwjtcTGAShqa8WktBXUmDqQxrVC4Y4Kw4SrnWQnxeVOtwuw1tvoNxDvdQCvHy9C7DXEyZvBapJfc2y6yihVyRpaZg3HrbRtNiCNyVofd1rbGB4j6Y1PJueE0YY5aUoYpTyHExn98A-6DnMcc1JNGSaKYK5opj7tqPyJKUXrDgYJ1n8a1IcGM_t-rzi3G9sdyL-VPY38DbG38QA01192EnrbuUy9-y-1n_IAyy6oHQ</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Yin, Dexin</creator><creator>Li, Yezhou</creator><creator>Fu, Changgeng</creator><creator>Feng, Ye</creator><general>S. 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metabolism</topic><topic>Atherosclerosis</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Line</topic><topic>Cell Movement</topic><topic>Cell Survival</topic><topic>DNA methylation</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelial Cells - metabolism</topic><topic>HMEC-1 cell</topic><topic>Humans</topic><topic>Kinases</topic><topic>Liver cancer</topic><topic>LncRNA HULC</topic><topic>MCL-1</topic><topic>MicroRNAs</topic><topic>MicroRNAs - antagonists & inhibitors</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miR-124</topic><topic>Myeloid Cell Leukemia Sequence 1 Protein - chemistry</topic><topic>Myeloid Cell Leukemia Sequence 1 Protein - genetics</topic><topic>Myeloid Cell Leukemia Sequence 1 Protein - metabolism</topic><topic>Neovascularization, Physiologic</topic><topic>Nitric oxide</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Retracted Paper</topic><topic>RNA Interference</topic><topic>RNA, Long Noncoding - antagonists & inhibitors</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Signal Transduction</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yin, Dexin</creatorcontrib><creatorcontrib>Li, Yezhou</creatorcontrib><creatorcontrib>Fu, Changgeng</creatorcontrib><creatorcontrib>Feng, Ye</creatorcontrib><collection>Karger 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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</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>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yin, Dexin</au><au>Li, Yezhou</au><au>Fu, Changgeng</au><au>Feng, Ye</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pro-Angiogenic Role of LncRNA HULC in Microvascular Endothelial Cells via Sequestrating miR-124</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>50</volume><issue>6</issue><spage>2188</spage><epage>2202</epage><pages>2188-2202</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>HULC is a multifunctional lncRNA that has pro-angiogenic function in various cancers. The present study was designed to see the role of lncRNA HULC in normal endothelial cells angiogenesis.
Cell viability, apoptosis, migration, tube formation and expression levels of angiogenesis-related proteins were respectively assessed in human microvascular endothelial HMEC-1 cells after lncRNA HULC was silenced by shRNA transfection. Cross-regulation between lncRNA HULC and miR-124, and between miR-124 and MCL-1 were detected by qRT-PCR, sequence analysis, and luciferase reporter assay.
Silence of lncRNA HULC significantly reduced viability, migration, tube formation and protein levels of VEGF, VEGFR2, CD144 and eNOS in HMEC-1 cells. Meanwhile, silence of lncRNA HULC induced apoptosis in HMEC-1 cells, as Bcl-2 was down-regulated, Bax was up-regulated, and caspase-3 and -9 were cleaved. miR-124 expression was negatively regulated by lncRNA HULC, and HULC worked as a molecular sponge for miR-124, in having miR-124 exhausted. Besides, MCL-1 was a target gene of miR-124. Rescue assay results showed that the effects of lncRNA HULC silence on HMEC-1 cells growth, migration and angiogenesis were abolished by miR-124 suppression. Similarly, the effects of miR-124 on HMEC-1 cells were abolished by MCL-1 overexpression. Furthermore, MCL-1 activated PI3K/AKT and JAK/STAT signaling pathways.
These findings suggest a pro-angiogenic role of lncRNA HULC in endothelial cells. The pro-angiogenic actions of lncRNA HULC may be through sponging miR-124, preventing MCL-1 from degradation by miR-124.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>30415256</pmid><doi>10.1159/000495060</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiogenesis Antagomirs - metabolism Atherosclerosis bcl-2-Associated X Protein - metabolism Caspase 3 - metabolism Cell Line Cell Movement Cell Survival DNA methylation Endothelial Cells - cytology Endothelial Cells - metabolism HMEC-1 cell Humans Kinases Liver cancer LncRNA HULC MCL-1 MicroRNAs MicroRNAs - antagonists & inhibitors MicroRNAs - genetics MicroRNAs - metabolism miR-124 Myeloid Cell Leukemia Sequence 1 Protein - chemistry Myeloid Cell Leukemia Sequence 1 Protein - genetics Myeloid Cell Leukemia Sequence 1 Protein - metabolism Neovascularization, Physiologic Nitric oxide Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Proto-Oncogene Proteins c-bcl-2 - metabolism Retracted Paper RNA Interference RNA, Long Noncoding - antagonists & inhibitors RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism RNA, Small Interfering - metabolism Signal Transduction STAT3 Transcription Factor - metabolism Vascular Endothelial Growth Factor A - metabolism |
| title | Pro-Angiogenic Role of LncRNA HULC in Microvascular Endothelial Cells via Sequestrating miR-124 |
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