English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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.

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