Non-coding RNAs as Regulators of Lymphangiogenesis in Lymphatic Development, Inflammation, and Cancer Metastasis.

Ming-Xin Cao,Xin-Hua Liang,Ya-Jie Tang,Wei-Long Zhang,Ya-Ling Tang

doi:10.3389/fonc.2019.00916

Abstract

Non-coding RNAs (ncRNAs), which do not encode proteins, have pivotal roles in manipulating gene expression in development, physiology, and pathology. Emerging data have shown that ncRNAs can regulate lymphangiogenesis, which refers to lymphatics deriving from preexisting vessels, becomes established during embryogenesis, and has a close relationship with pathological conditions such as lymphatic developmental diseases, inflammation, and cancer. This review summarizes the molecular mechanisms of lymphangiogenesis in lymphatic development, inflammation and cancer metastasis, and discusses ncRNAs' regulatory effects on them. Therapeutic targets with regard to lymphangiogenesis are also discussed.

Highlights

Lymphangiogenesis are termed lymphatics deriving from preexisting vessels, and generally progress through a number of stages: establishment of lymphatic endothelial cell (LEC) identity, formation of the primary lymphatic structures, maturation, and remodeling of the lymphatic vessels [1, 2]
Our comprehension of lymphangiogenesis regulation is mainly based on understanding the functions of proteins and their interactions, while it is widely known that only 3–5% of our genome encodes proteins and protein-target therapy may cause drug resistance [7]
Jones et al demonstrated that miR-1236, induced by Interleukine-1 beta (IL-1β), could negatively regulate vascular endothelial growth factor receptor-3 (VEGFR-3) expression and VEGFR-3-dependent signaling Akt and ERK1/2, and attenuate vascular endothelial growth factor C (VEGF-C)/VEGFR-3 mediated LECs migration and tube formation in primary human LECs in vitro

Summary

Introduction

Lymphangiogenesis are termed lymphatics deriving from preexisting vessels, and generally progress through a number of stages: establishment of lymphatic endothelial cell (LEC) identity, formation of the primary lymphatic structures, maturation, and remodeling of the lymphatic vessels [1, 2]. Jones et al demonstrated that miR-1236, induced by IL-1β, could negatively regulate VEGFR-3 expression and VEGFR-3-dependent signaling Akt and ERK1/2, and attenuate VEGF-C/VEGFR-3 mediated LECs migration and tube formation in primary human LECs in vitro.

Results

Conclusion