{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hu X"],"funding":["National Natural Science Foundation of China","National College Student Innovation Training Project of Anhui Medical University","Key Research and Development Projects in Anhui Province"],"pagination":["897-905"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8024507"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["246(8)"],"pubmed_abstract":["Excessive proliferation of vascular endothelial cells can cause hemangioma. Although typically benign, hemangiomas can become life-threatening. The microRNA miR-200c-3p is abnormally expressed in some types of tumors, but its expression, biological role, and mechanism of action in infantile hemangioma remain to be fully elucidated. The expression levels of miR-200c-3p in hemangioma tissue were compared with those in adjacent healthy tissue by using bioinformatics analyses and TargetScan. Western blot, enzyme-linked immunosorbent assay, and Cell Counting Kit 8 analyses were used to determine the biological function and site of action of miR-200c-3p in human dermal microvascular endothelial cells (HDMECs). MiR-200c-3p was one of the top 10 differentially expressed genes between healthy tissue, and hemangiomas tissues, having markedly decreased expression in hemangioma tissue. Reduction of miR-200c-3p expression in HDMECs through the transfection of a miR-200c-3p inhibitor significantly increased HDMEC proliferation. The addition of the Notch signaling pathway inhibitor DAPT to HDMECs transfected with the miR-200c-3p inhibitor eliminated the inhibitor-induced enhancement of proliferation in HDMECs. These findings indicate that miR-200c-3p targets the Notch signaling pathway to promote the proliferation of vascular endothelial cells, suggesting that miR-200c-3p plays an important role in the pathogenesis of hemangioma."],"journal":["Experimental biology and medicine (Maywood, N.J.)"],"pubmed_title":["MiR-200c-3p increased HDMEC proliferation through the notch signaling pathway."],"pmcid":["PMC8024507"],"funding_grant_id":["201910366002","202004j07020034","U1732157","8197102295"],"pubmed_authors":["Bai S","Wang S","Hu X","Zhang N","Shen B","Du J","Liu S","Li L","Tian P"],"additional_accession":[]},"is_claimable":false,"name":"MiR-200c-3p increased HDMEC proliferation through the notch signaling pathway.","description":"Excessive proliferation of vascular endothelial cells can cause hemangioma. Although typically benign, hemangiomas can become life-threatening. The microRNA miR-200c-3p is abnormally expressed in some types of tumors, but its expression, biological role, and mechanism of action in infantile hemangioma remain to be fully elucidated. The expression levels of miR-200c-3p in hemangioma tissue were compared with those in adjacent healthy tissue by using bioinformatics analyses and TargetScan. Western blot, enzyme-linked immunosorbent assay, and Cell Counting Kit 8 analyses were used to determine the biological function and site of action of miR-200c-3p in human dermal microvascular endothelial cells (HDMECs). MiR-200c-3p was one of the top 10 differentially expressed genes between healthy tissue, and hemangiomas tissues, having markedly decreased expression in hemangioma tissue. Reduction of miR-200c-3p expression in HDMECs through the transfection of a miR-200c-3p inhibitor significantly increased HDMEC proliferation. The addition of the Notch signaling pathway inhibitor DAPT to HDMECs transfected with the miR-200c-3p inhibitor eliminated the inhibitor-induced enhancement of proliferation in HDMECs. These findings indicate that miR-200c-3p targets the Notch signaling pathway to promote the proliferation of vascular endothelial cells, suggesting that miR-200c-3p plays an important role in the pathogenesis of hemangioma.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Apr","modification":"2025-04-29T11:33:34.363Z","creation":"2025-04-06T19:54:42.632Z"},"accession":"S-EPMC8024507","cross_references":{"pubmed":["33472424"],"doi":["10.1177/1535370220981859"]}}