MicroRNAs modulate the angiogenic properties of HUVECs

Poliseno, Laura; Tuccoli, Andrea; Mariani, Laura; Evangelista, Monica; Citti, Lorenzo; Woods, Keith; Mercatanti, Alberto; Hammond, Scott M.; Rainaldi, Giuseppe

doi:10.1182/blood-2006-01-012369

Cited by 682 publications

(576 citation statements)

References 25 publications

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“…Recent reports revealed that the receptor tyrosine kinase Kit and the cyclin-dependent kinase (cdk) inhibitor, p27 kip1 , are both miR-221 and -222 functional targets (Felli et al, 2005;He et al, 2005;Poliseno et al, 2006;le Sage et al, 2007). Here we demonstrate that silencing of p27 kip1 , but not of Kit, increases TRAIL resistance.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA signatures of TRAIL resistance in human non-small cell lung cancer

et al. 2008

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To define novel pathways that regulate susceptibility to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in non-small cell lung cancer (NSCLC), we have performed genome-wide expression profiling of microRNAs (miRs). We show that in TRAIL-resistant NSCLC cells, levels of different miRs are increased, and in particular, miR-221 and -222. We demonstrate that these miRs impair TRAIL-dependent apoptosis by inhibiting the expression of key functional proteins. Indeed, transfection with anti-miR-221 and -222 rendered CALU-1-resistant cells sensitive to TRAIL. Conversely, H460-sensitive cells treated with -221 and -222 pre-miRs become resistant to TRAIL. miR-221 and -222 target the 3 0 -UTR of Kit and p27 kip1 mRNAs, but interfere with TRAIL signaling mainly through p27 kip1 . In conclusion, we show that high expression levels of miR-221 and -222 are needed to maintain the TRAIL-resistant phenotype, thus making these miRs as promising therapeutic targets or diagnostic tool for TRAIL resistance in NSCLC.

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Section: Discussionmentioning

confidence: 99%

MicroRNA signatures of TRAIL resistance in human non-small cell lung cancer

et al. 2008

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“…In the absence of activating mutations in KIT, this paracrine stimulation may be the basis for tumor proliferation in Merkel cell carcinoma. Alternatively, downregulation of miRNAs, such as miRNA-221 and miRNA-222 which regulate KIT expression by binding to its 3 0 -UTR, 34,45,46 or an unknown mutation in the miRNA recognition site, can also result in receptor expression in the absence of gene amplification or mutations in KIT. This posttranscriptional regulation may also explain the absence of KIT expression in some of our cases of Merkel cell carcinoma, even in the presence of lesional SCF.…”

Section: Discussionmentioning

confidence: 99%

Silent mutations in KIT and PDGFRA and coexpression of receptors with SCF and PDGFA in Merkel cell carcinoma: implications for tyrosine kinase-based tumorigenesis

Kartha

Sundram

2008

Modern Pathology

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Merkel cell carcinoma is a rare and aggressive form of skin cancer of neuroendocrine origin. Its treatment involves wide excision and radiotherapy but no effective therapy exists for advanced disease. Upregulation of the platelet-derived growth factor receptor family of tyrosine kinases, PDGFRA and KIT, has a crucial role in cancer development. Several studies have shown expression of the tyrosine kinase receptor KIT (CD117) in Merkel cell carcinoma. In this study, we examined the expression and mutational status of KIT and PDGFRA in 14 primary and 18 metastatic Merkel cell carcinoma. The expression of KIT and PDGFRA and their respective ligands, stem cell factor (SCF) and PDGFA, was assessed by immunohistochemistry. In addition, we analyzed KIT exons 9, 11, 13 and 17, and PDGFRA exons 10, 12 and 18 for the presence of activating mutations. We found that only 53% of cases of Merkel cell carcinoma expressed KIT, which was mostly seen as diffuse weak staining, and SCF expression was observed only in 31% of cases. In contrast, 87 and 81% of cases expressed PDGFRA and PDGFA, respectively. We observed coexpression of SCF and KIT in only 5 of 32 cases (16%) whereas 25 of 31 cases (81%) showed coexpression of PDGFRA and its ligand PDGFA. While we documented silent mutations in exon 17 of KIT and exons 10, 12 and 18 of PDGFRA, we were not able to identify any known activating mutations. Our results indicate that there is no correlation between positive immunostaining and occurrence of activating mutations in KIT and PDGFRA. Moreover, the presence of KIT/SCF and PDGFRA/PDGFA coexpression in a proportion of cases may indicate an autocrine/paracrine stimulation loop. We think therefore that imatinib mesylate is less likely to be an effective therapy for Merkel cell carcinoma, unless activating mutations exist in other exons of these receptor kinases.

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“…Many studies reported that miR‐221 and miR‐222 have the effect of promoting and/or inhibiting tumour angiogenesis in the malignant processes of HCC,62 breast cancer,63 lung cancer,64 human epithelial cancers,65 human glioblastoma,66 gastric cancer 67 and other various cancers 60, 61, 68, 69, 70, 71. MiR‐221 and miR‐222 inhibit angiogenesis by blocking tube formation, proliferation, migration and wound healing through repressing the expression of c‐Kit and endothelial nitric oxide synthase (eNOS) 24, 26, 72, 73. Moreover, they both suppress angiogenesis by reducing zinc finger E‐box binding homeobox 2 (ZEB2) in ECs 74…”

Section: Mirnas That Target Genes Involved In Angiogenesismentioning

confidence: 99%

The regulatory role of microRNAs in angiogenesis‐related diseases

Sun

Lei

et al. 2018

J Cellular Molecular Medi

119

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MicroRNAs (miRNAs) are small non‐coding RNAs that regulate gene expression at a post‐transcriptional level via either the degradation or translational repression of a target mRNA. They play an irreplaceable role in angiogenesis by regulating the proliferation, differentiation, apoptosis, migration and tube formation of angiogenesis‐related cells, which are indispensable for multitudinous physiological and pathological processes, especially for the occurrence and development of vascular diseases. Imbalance between the regulation of miRNAs and angiogenesis may cause many diseases such as cancer, cardiovascular disease, aneurysm, Kawasaki disease, aortic dissection, phlebothrombosis and diabetic microvascular complication. Therefore, it is important to explore the essential role of miRNAs in angiogenesis, which might help to uncover new and effective therapeutic strategies for vascular diseases. This review focuses on the interactions between miRNAs and angiogenesis, and miRNA‐based biomarkers in the diagnosis, treatment and prognosis of angiogenesis‐related diseases, providing an update on the understanding of the clinical value of miRNAs in targeting angiogenesis.

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MicroRNAs modulate the angiogenic properties of HUVECs

Cited by 682 publications

References 25 publications

MicroRNA signatures of TRAIL resistance in human non-small cell lung cancer

MicroRNA signatures of TRAIL resistance in human non-small cell lung cancer

Silent mutations in KIT and PDGFRA and coexpression of receptors with SCF and PDGFA in Merkel cell carcinoma: implications for tyrosine kinase-based tumorigenesis

The regulatory role of microRNAs in angiogenesis‐related diseases

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