Mechanism of miR-503-5p on cardiac hemangioma and clinical validation.

IF 3.6 3区 医学 Q2 ONCOLOGY
American journal of cancer research Pub Date : 2024-11-15 eCollection Date: 2024-01-01 DOI:10.62347/EVMG4299
Kai Lu, Wanchao Zhang, Xiaoqiang Tang, Ruohan Yin, Tao Wang, Xiaoyu Wei, Changjie Pan
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引用次数: 0

Abstract

It has been claimed that microRNA 503-5p (miR-503-5p) is the key to the future diagnosis and treatment of cardiac hemangioma (CH), but the relationship between the two has not been fully validated. In this study, we analyzed the effect of miR-503-5p targeting type IA bone morphogenetic protein receptor (BMPR1A) on CH to inform future diagnosis and treatment of CH. First, miR-503-5p and BMPR1A abnormal expression sequences (vectors) were transfected into human hemangioma-derived endothelial cells (HemECs) and human umbilical vein endothelial cells (HUVECs) to observe alterations in cell biological behavior, adhesion, and epithelial mesenchymal transition (EMT). We found enhanced proliferative, invasive and migrating abilities of HemECs and HUVECs after silencing miR-503-5p or increasing BMPR1A, accompanied by reduced apoptosis, elevated intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), and accelerated EMT; after increasing miR-503-5p or silencing BMPR1A, the cells exhibited reduced apoptosis, elevated ICAM-1 and VCAM-1, and accelerated EMT (P<0.05). Subsequently, a dual-luciferase reporter assay was performed to analyze the targeting relationship between miR-503-5p and BMPR1A. The results showed that miR-503-5p inhibited BMPR1A-wild type (WT) fluorescence activity (P<0.05). Through the rescue experiment, it was observed that the biological behavior of the cells with simultaneous elevation or simultaneous silencing of miR-503-5p and BMPR1A was not different from that of cells transfected with BMPR1A empty vector (P>0.05), indicating that the effect of BMPR1A on cells was reversed by miR-503-5p. Finally, in the analysis of clinical records, we found that CH cases exhibited lower miR-503-5p and higher BMPR1A levels than healthy controls (P<0.05). The expression of the two genes was negatively correlated (P<0.05). These results suggest that miR-503-5p participates in CH growth by targeted sponging of BMPR1A.

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来源期刊
自引率
3.80%
发文量
263
期刊介绍: The American Journal of Cancer Research (AJCR) (ISSN 2156-6976), is an independent open access, online only journal to facilitate rapid dissemination of novel discoveries in basic science and treatment of cancer. It was founded by a group of scientists for cancer research and clinical academic oncologists from around the world, who are devoted to the promotion and advancement of our understanding of the cancer and its treatment. The scope of AJCR is intended to encompass that of multi-disciplinary researchers from any scientific discipline where the primary focus of the research is to increase and integrate knowledge about etiology and molecular mechanisms of carcinogenesis with the ultimate aim of advancing the cure and prevention of this increasingly devastating disease. To achieve these aims AJCR will publish review articles, original articles and new techniques in cancer research and therapy. It will also publish hypothesis, case reports and letter to the editor. Unlike most other open access online journals, AJCR will keep most of the traditional features of paper print that we are all familiar with, such as continuous volume, issue numbers, as well as continuous page numbers to retain our comfortable familiarity towards an academic journal.
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