Dataset Information

MiR-93-5p enhances growth and angiogenesis capacity of HUVECs by down-regulating EPLIN.

ABSTRACT: Tumor angiogenesis is essential in delivering oxygen and nutrients to growing tumors, and therefore considered as a hallmark of cancer. MicroRNAs (miRNAs) have been shown to play important roles in regulating tumor angiogenesis. MicroRNA-93-5p (miR-93-5p) has been identified as an oncogenic miRNA in a variety of human malignancies and involved in tumor angiogenesis in astrocytoma. However, the direct effect(s) of miR-93-5p on the biological behaviors of endothelial cells have not been investigated. Thus, in the present study we investigated the role(s) of miR-93-5p in regulating the functions of human umbilical vein endothelial cells (HUVECs). We found that triple negative breast cancer (TNBC) tissues with higher levels of miR-93-5p showed higher blood vessel density. Overexpression of miR-93-5p accelerated HUVECs proliferation and migration and promoted HUVECs lumen formation and sprouting in vitro, while blockade of miR-93-5p suppressed HUVECs migration and angiogenic capacity. The mechanistic studies revealed that miR-93-5p can promote angiogenic process through inhibiting epithelial protein lost in neoplasm (EPLIN) expression in HUVECs. In sum, our results have indicated that miR-93-5p promoted angiogenesis through down-regulating EPLIN and therefore represented a promising target for developing novel anti-angiogenic therapeutics.

SUBMITTER: Liang L

PROVIDER: S-EPMC5739794 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

MiR-93-5p enhances growth and angiogenesis capacity of HUVECs by down-regulating EPLIN.

Liang Liang L Zhao Lei L Zan Ying Y Zhu Qing Q Ren Juan J Zhao Xinhan X

Oncotarget 20171106 63

Tumor angiogenesis is essential in delivering oxygen and nutrients to growing tumors, and therefore considered as a hallmark of cancer. MicroRNAs (miRNAs) have been shown to play important roles in regulating tumor angiogenesis. MicroRNA-93-5p (miR-93-5p) has been identified as an oncogenic miRNA in a variety of human malignancies and involved in tumor angiogenesis in astrocytoma. However, the direct effect(s) of miR-93-5p on the biological behaviors of endothelial cells have not been investigat ...[more]

PMID: 29291009

Similar Datasets

Project description:BackgroundNontraumatic osteonecrosis of the femoral head (NONFH) is a common, progressive, and refractory orthopaedic disease. Decreased osteogenesis and angiogenesis are considered the main factors in the pathogenesis of NONFH. We aimed to figure out whether exosomes and exosomal miRNA from necrotic bone tissues of patients with NONFH are involved in the pathogenesis of NONFH and reveal the underlying mechanisms.MethodsRT-PCR and western blotting (WB) were used to detect the expression of osteogenic, adipogenic, and angiogenic markers. ALP staining and Alizarin Red S (ARS) staining were used to evaluate osteogenic differentiation of human bone marrow-derived mesenchymal stem cells (hBMSCs). Oil Red O staining was performed to assess the adipocyte deposition. A tube formation assay was used to study angiogenesis of human umbilical vascular endothelial cells (HUVECs). H&E staining and immunohistochemistry (IHC) staining were used to detect the effect of the NONFH exosomes in vivo. MicroRNA sequencing was conducted to identify potential regulators in the NONFH exosomes. The target relationship between miR-100-5p and BMPR2 was predicted and confirmed by a dual luciferase reporter assay and WB.ResultsThe NONFH exosomes reduced the osteogenic differentiation of hBMSCs and angiogenesis of HUVECs. In addition, the injection of the NONFH exosomes caused thinning and disruption of bone trabeculae in the femoral heads of rats. MiR-100-5p expression was upregulated in the NONFH exosomes and inhibited the osteogenesis of hBMSCs and angiogenesis of HUVECs by targeting BMPR2 and suppressing the BMPR2/SMAD1/5/9 signalling pathway. Silencing miR-100-5p expression rescued the reduction in osteogenesis and angiogenesis caused by the NONFH exosomes by activating the BMPR2/SMAD1/5/9 signalling pathway.ConclusionThe NONFH exosomal miR-100-5p can lead to NONFH-like damage by targeting BMPR2 and suppressing the BMPR2/SMAD1/5/9 signalling pathway, which may be involved in the pathophysiological mechanisms of nontraumatic osteonecrosis of the femoral head (NONFH).

Dataset Information

MiR-93-5p enhances growth and angiogenesis capacity of HUVECs by down-regulating EPLIN.

Publications

MiR-93-5p enhances growth and angiogenesis capacity of HUVECs by down-regulating EPLIN.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets