Abstract
Angiogenesis is one of the hallmarks of cancer, and the establishment of new blood vessels is vital to allow for a tumour to grow beyond 1–2 mm in size. The angiogenic switch is the term given to the point where the number or activity of the pro-angiogenic factors exceeds that of the anti-angiogenic factors, resulting in the angiogenic process proceeding, giving rise to new blood vessels accompanied by increased tumour growth, metastasis, and potential drug resistance. Long noncoding ribonucleic acids (lncRNAs) have been found to play a role in the angiogenic switch by regulating gene expression, transcription, translation, and post translation modification. In this regard they play both anti-angiogenic and pro-angiogenic roles. The expression levels of the pro-angiogenic lncRNAs have been found to correlate with patient survival. These lncRNAs are also potential drug targets for the development of therapies that will inhibit or modify tumour angiogenesis. Here we review the roles of lncRNAs in regulating the angiogenic switch. We cover specific examples of both pro and anti-angiogenic lncRNAs and discuss their potential use as both prognostic biomarkers and targets for the development of future therapies.
Highlights
Over the years the focus of cancer treatment has largely been on eliminating neoplastic cells
It is evident from emerging studies that Long noncoding ribonucleic acids (lncRNAs) regulate the fine balance between proand antiangiogenic factors, and that their deregulation may contribute to the transition from the dormant avascular tumour to an angiogenic malignant phenotype
Future investigations should focus on the sensitivity and specificity of Metastasis-associated lung adeno-carcinoma transcript 1 (MALAT1) and H19 in cancer detection
Summary
Over the years the focus of cancer treatment has largely been on eliminating neoplastic cells. LncRNAs, which regulate the process of blood vessel formation include myocardial infarction associated transcript (MIAT), which functions as a miR-150-5p sponge to regulate vascular endothelial growth factor (VEGF) expression [6,8,9,10]. Spliced transcript—endothelial-enriched lncRNA (STEEL) regulates physiological angiogenesis by transcriptionally reducing the expression of endothelial nitric oxide synthase (eNOS) and other EC function modulators such as Kruppel-like Factor 2 (KLF2) [10]. Another lncRNA, MANTIS, known as lncRNA n342419, regulates vascularisation mainly in response to changes in blood flow patterns [8,9]. Aberrant expression of lncRNAs in endothelial cells is observed in various diseases, including cancer [5,7]
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