The Mechanism of Oxymatrine Targeting miR-27a-3p/PPAR-γ Signaling Pathway through m6A Modification to Regulate the Influence on Hemangioma Stem Cells on Propranolol Resistance
Objective: The proliferation and migration of hemangioma stem cells (HemSCs) induced apoptosis and adipose differentiation as well as increased the sensitivity of HemSCs to propranolol (PPNL). MiR-27a-3p negatively controlled the peroxisome-proliferator-activated receptor γ (PPAR-γ) level, counterac...
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| Veröffentlicht in: | Cancers 2023-11, Vol.15 (21), p.5213 |
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| creator | Dai, Yuxin Qiu, Mingke Zhang, Shenglai Peng, Jingyu Hou, Xin Liu, Jie Li, Feifei Ou, Jingmin |
| description | Objective: The proliferation and migration of hemangioma stem cells (HemSCs) induced apoptosis and adipose differentiation as well as increased the sensitivity of HemSCs to propranolol (PPNL). MiR-27a-3p negatively controlled the peroxisome-proliferator-activated receptor γ (PPAR-γ) level, counteracting the effect of PPAR-γ on HemSC progression and PPNL resistance. OMT accelerated HemSC progression and adipocyte differentiation via modulating the miR-27a-3p/PPAR-γ axis, inhibiting HemSC resistance to PPNL. In tumor-forming experiments, OMT exhibited a dose-dependent inhibitory effect on the volume of IH PPNL-resistant tumors, which was partially dependent on the regulation of m6A methylation transfer enzyme METTL3 and the miR-27a-3p/PPAR-γ axis, thereby inducing apoptosis. Conclusions: We conclude that OMT regulates IH and influences PPNL resistance via targeting the miR-27a-3p/PPAR-γ signaling pathway through m6A modification. |
| doi_str_mv | 10.3390/cancers15215213 |
| format | Article |
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MiR-27a-3p negatively controlled the peroxisome-proliferator-activated receptor γ (PPAR-γ) level, counteracting the effect of PPAR-γ on HemSC progression and PPNL resistance. OMT accelerated HemSC progression and adipocyte differentiation via modulating the miR-27a-3p/PPAR-γ axis, inhibiting HemSC resistance to PPNL. In tumor-forming experiments, OMT exhibited a dose-dependent inhibitory effect on the volume of IH PPNL-resistant tumors, which was partially dependent on the regulation of m6A methylation transfer enzyme METTL3 and the miR-27a-3p/PPAR-γ axis, thereby inducing apoptosis. Conclusions: We conclude that OMT regulates IH and influences PPNL resistance via targeting the miR-27a-3p/PPAR-γ signaling pathway through m6A modification.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers15215213</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Adipocytes ; Antibodies ; Apoptosis ; Biotechnology ; Cell death ; Cell differentiation ; Cell migration ; Cell proliferation ; Ethics ; Health aspects ; Hemangioma ; Methylation ; Methyltransferases ; MicroRNAs ; N6-methyladenosine ; Pathogenesis ; Peroxisome proliferator-activated receptors ; Propranolol ; Propranolol hydrochloride ; Signal transduction ; Stem cell research ; Stem cells ; Tumors</subject><ispartof>Cancers, 2023-11, Vol.15 (21), p.5213</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c364t-10a44f554c21080d3fbe8cc747c8d23c5ff2a374aca5564c97ee83b3c34417aa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids></links><search><creatorcontrib>Dai, Yuxin</creatorcontrib><creatorcontrib>Qiu, Mingke</creatorcontrib><creatorcontrib>Zhang, Shenglai</creatorcontrib><creatorcontrib>Peng, Jingyu</creatorcontrib><creatorcontrib>Hou, Xin</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Li, Feifei</creatorcontrib><creatorcontrib>Ou, Jingmin</creatorcontrib><title>The Mechanism of Oxymatrine Targeting miR-27a-3p/PPAR-γ Signaling Pathway through m6A Modification to Regulate the Influence on Hemangioma Stem Cells on Propranolol Resistance</title><title>Cancers</title><description>Objective: The proliferation and migration of hemangioma stem cells (HemSCs) induced apoptosis and adipose differentiation as well as increased the sensitivity of HemSCs to propranolol (PPNL). MiR-27a-3p negatively controlled the peroxisome-proliferator-activated receptor γ (PPAR-γ) level, counteracting the effect of PPAR-γ on HemSC progression and PPNL resistance. OMT accelerated HemSC progression and adipocyte differentiation via modulating the miR-27a-3p/PPAR-γ axis, inhibiting HemSC resistance to PPNL. In tumor-forming experiments, OMT exhibited a dose-dependent inhibitory effect on the volume of IH PPNL-resistant tumors, which was partially dependent on the regulation of m6A methylation transfer enzyme METTL3 and the miR-27a-3p/PPAR-γ axis, thereby inducing apoptosis. Conclusions: We conclude that OMT regulates IH and influences PPNL resistance via targeting the miR-27a-3p/PPAR-γ signaling pathway through m6A modification.</description><subject>Adipocytes</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Biotechnology</subject><subject>Cell death</subject><subject>Cell differentiation</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Ethics</subject><subject>Health aspects</subject><subject>Hemangioma</subject><subject>Methylation</subject><subject>Methyltransferases</subject><subject>MicroRNAs</subject><subject>N6-methyladenosine</subject><subject>Pathogenesis</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Propranolol</subject><subject>Propranolol hydrochloride</subject><subject>Signal transduction</subject><subject>Stem cell research</subject><subject>Stem cells</subject><subject>Tumors</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><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>eNptksFq3DAQhk1poSHNuVdBL704a0uypT0uS9sEErJstmcz0Y5sBUvaSjLNvlWh75FnitwU2oaOBBL6v38YSVMU7-vqnLFltVDgFIZYN3Se7FVxQitBy7Zd8td_7d8WZzHeVzkYq0UrToofuwHJNaoBnImWeE1uHo4WUjAOyQ5Cj8m4nlizLamAkh0Wm81qWz7-JLemdzDO4gbS8B2OJA3BT_1AbLsi135vtFGQjHckebLFfhohYYaQXDo9TpgrJlm8QAuuN94CuU1oyRrHMc7CJvhDAOdHP2Z7NDHNl3xXvNEwRjz7vZ4WXz9_2q0vyqubL5fr1VWpWMtTWVfAuW4armhdyWrP9B1KpQQXSu4pU43WFJjgoKBpWq6WAlGyO6YY57UAYKfFx-e8h-C_TRhTZ01UuTZw6KfYUSmXOZq6zuiHF-i9n0J-nF-UrLhkQv6hehixM077FEDNSbuVELTJHyJn6vw_VB57tEZ5h9rk838Mi2eDCj7GgLo7BGMhHLu66ube6F70BnsCH3-uNQ</recordid><startdate>20231101</startdate><enddate>20231101</enddate><creator>Dai, Yuxin</creator><creator>Qiu, Mingke</creator><creator>Zhang, Shenglai</creator><creator>Peng, Jingyu</creator><creator>Hou, Xin</creator><creator>Liu, Jie</creator><creator>Li, Feifei</creator><creator>Ou, Jingmin</creator><general>MDPI AG</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20231101</creationdate><title>The Mechanism of Oxymatrine Targeting miR-27a-3p/PPAR-γ Signaling Pathway through m6A Modification to Regulate the Influence on Hemangioma Stem Cells on Propranolol Resistance</title><author>Dai, Yuxin ; Qiu, Mingke ; Zhang, Shenglai ; Peng, Jingyu ; Hou, Xin ; Liu, Jie ; Li, Feifei ; Ou, Jingmin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c364t-10a44f554c21080d3fbe8cc747c8d23c5ff2a374aca5564c97ee83b3c34417aa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Adipocytes</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Biotechnology</topic><topic>Cell death</topic><topic>Cell differentiation</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Ethics</topic><topic>Health aspects</topic><topic>Hemangioma</topic><topic>Methylation</topic><topic>Methyltransferases</topic><topic>MicroRNAs</topic><topic>N6-methyladenosine</topic><topic>Pathogenesis</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Propranolol</topic><topic>Propranolol hydrochloride</topic><topic>Signal transduction</topic><topic>Stem cell research</topic><topic>Stem cells</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dai, Yuxin</creatorcontrib><creatorcontrib>Qiu, Mingke</creatorcontrib><creatorcontrib>Zhang, Shenglai</creatorcontrib><creatorcontrib>Peng, Jingyu</creatorcontrib><creatorcontrib>Hou, Xin</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Li, Feifei</creatorcontrib><creatorcontrib>Ou, Jingmin</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content 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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dai, Yuxin</au><au>Qiu, Mingke</au><au>Zhang, Shenglai</au><au>Peng, Jingyu</au><au>Hou, Xin</au><au>Liu, Jie</au><au>Li, Feifei</au><au>Ou, Jingmin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Mechanism of Oxymatrine Targeting miR-27a-3p/PPAR-γ Signaling Pathway through m6A Modification to Regulate the Influence on Hemangioma Stem Cells on Propranolol Resistance</atitle><jtitle>Cancers</jtitle><date>2023-11-01</date><risdate>2023</risdate><volume>15</volume><issue>21</issue><spage>5213</spage><pages>5213-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Objective: The proliferation and migration of hemangioma stem cells (HemSCs) induced apoptosis and adipose differentiation as well as increased the sensitivity of HemSCs to propranolol (PPNL). MiR-27a-3p negatively controlled the peroxisome-proliferator-activated receptor γ (PPAR-γ) level, counteracting the effect of PPAR-γ on HemSC progression and PPNL resistance. OMT accelerated HemSC progression and adipocyte differentiation via modulating the miR-27a-3p/PPAR-γ axis, inhibiting HemSC resistance to PPNL. In tumor-forming experiments, OMT exhibited a dose-dependent inhibitory effect on the volume of IH PPNL-resistant tumors, which was partially dependent on the regulation of m6A methylation transfer enzyme METTL3 and the miR-27a-3p/PPAR-γ axis, thereby inducing apoptosis. Conclusions: We conclude that OMT regulates IH and influences PPNL resistance via targeting the miR-27a-3p/PPAR-γ signaling pathway through m6A modification.</abstract><cop>Basel</cop><pub>MDPI AG</pub><doi>10.3390/cancers15215213</doi><oa>free_for_read</oa></addata></record> |
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| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; MDPI - Multidisciplinary Digital Publishing Institute; PubMed Central |
| subjects | Adipocytes Antibodies Apoptosis Biotechnology Cell death Cell differentiation Cell migration Cell proliferation Ethics Health aspects Hemangioma Methylation Methyltransferases MicroRNAs N6-methyladenosine Pathogenesis Peroxisome proliferator-activated receptors Propranolol Propranolol hydrochloride Signal transduction Stem cell research Stem cells Tumors |
| title | The Mechanism of Oxymatrine Targeting miR-27a-3p/PPAR-γ Signaling Pathway through m6A Modification to Regulate the Influence on Hemangioma Stem Cells on Propranolol Resistance |
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