Anti-miRNA oligonucleotides: A comprehensive guide for design

Lima, J. J. G.; Cerqueira, Laura; Figueiredo, Céu; Oliveira, Carla; Azevedo, Nuno F.

doi:10.1080/15476286.2018.1445959

Cited by 201 publications

(173 citation statements)

References 138 publications

(170 reference statements)

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“…Recently, experimental evidence has shown the potential use of antisense oligonucleotides to suppress aberrant miRNA function (AMOs) in several human pathologies, and hence the design of specific AMO-based strategies could find future application as RNA-based therapy that could prevent or at least to delay the onset of MEN 1-associated tumors [ 88 ].…”

Section: Discussionmentioning

confidence: 99%

Multiple Endocrine Neoplasia Type 1: The Potential Role of microRNAs in the Management of the Syndrome

Donati

Ciuffi²,

Marini³

et al. 2020

IJMS

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Multiple endocrine neoplasia type 1 (MEN1) is a rare inherited tumor syndrome, characterized by the development of multiple neuroendocrine tumors (NETs) in a single patient. Major manifestations include primary hyperparathyroidism, gastro-entero-pancreatic neuroendocrine tumors, and pituitary adenomas. In addition to these main NETs, various combinations of more than 20 endocrine and non-endocrine tumors have been described in MEN1 patients. Despite advances in diagnostic techniques and treatment options, which are generally similar to those of sporadic tumors, patients with MEN1 have a poor life expectancy, and the need for targeted therapies is strongly felt. MEN1 is caused by germline heterozygous inactivating mutations of the MEN1 gene, which encodes menin, a tumor suppressor protein. The lack of a direct genotype–phenotype correlation does not permit the determination of the exact clinical course of the syndrome. One of the possible causes of this lack of association could be ascribed to epigenetic factors, including microRNAs (miRNAs), single-stranded non-coding small RNAs that negatively regulate post-transcriptional gene expression. Some miRNAs, and their deregulation, have been associated with MEN1 tumorigenesis. Recently, an extracellular class of miRNAs has also been identified (c-miRNAs); variations in their levels showed association with various human diseases, including tumors. The aim of this review is to provide a general overview on the involvement of miRNAs in MEN1 tumor development, to be used as possible targets for novel molecular therapies. The potential role of c-miRNAs as future non-invasive diagnostic and prognostic biomarkers of MEN1 will be discussed as well.

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Section: Discussionmentioning

confidence: 99%

Multiple Endocrine Neoplasia Type 1: The Potential Role of microRNAs in the Management of the Syndrome

Donati

Ciuffi²,

Marini³

et al. 2020

IJMS

View full text Add to dashboard Cite

show abstract

“…Currently, there are two strategies to miRNA therapeutics [463,464]; 1) directly, by inhibiting onco-miRs using miRNA antagonists, or indirectly, by utilizing miRNAs or non-miRNA targets that are known to downregulate the specific onco-miRs, and 2) to restore the loss-of-function of ts-miRNAs using ts-miR mimetics. Table 2 shows a summary of the different types of miRNA-based therapies for breast cancer treatment.…”

Section: Mirna-based Therapeuticsmentioning

confidence: 99%

Potential miRNAs for miRNA-Based Therapeutics in Breast Cancer

Wong

Cheah

2020

ncRNA

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MicroRNAs (miRNAs) are small non-coding RNAs that can post-transcriptionally regulate the genes involved in critical cellular processes. The aberrant expressions of oncogenic or tumor suppressor miRNAs have been associated with cancer progression and malignancies. This resulted in the dysregulation of signaling pathways involved in cell proliferation, apoptosis and survival, metastasis, cancer recurrence and chemoresistance. In this review, we will first (i) provide an overview of the miRNA biogenesis pathways, and in vitro and in vivo models for research, (ii) summarize the most recent findings on the roles of microRNAs (miRNAs) that could potentially be used for miRNA-based therapy in the treatment of breast cancer and (iii) discuss the various therapeutic applications.

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“…Antisense microRNAs are used to target aberrant miRNA [43]. We used antagomir (amiR) 103 and amiR-107 to test the hypothesis that silencing amylin-induced upregulation of miR-103 and miR-107 rescues LRP1 expression.…”

Section: Antisense Micrornas Rescue Amylin-induced Suppression Of Aβ mentioning

confidence: 99%

Amylin-mediated regulation of LRP1 by miR-103/107 induces cerebral microvascular dysfunction and impairs β-amyloid efflux

Velmurugan¹,

Ly²,

Sharma³

et al. 2020

Preprint

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Background: The cerebral small blood vessels of individuals with Alzheimer’s Disease (AD) often have deposits of amylin, an amyloid-forming protein secreted in the blood by pancreatic β-cells. To determine whether systemic pancreatic amylin dyshomeostasis impairs amyloid β (Aβ) efflux across the blood-brain barrier (BBB), we studied cerebral microvessels in humans and rats with pancreatic expression of amyloidogenic human amylin, and evaluated the effect of human amylin in an in vitro BBB model. Methods: Brain sections from AD and cognitively unimpaired individuals were co-stained with anti-Aβ and anti-amylin antibodies. In vivo analyses of Aβ efflux across the BBB were carried out in aged rats that express amyloid-forming human amylin in pancreatic β-cells and littermates expressing non-amyloidogenic rat amylin. We also used an in vitro BBB model of Aβ transcytosis in which the endothelial cell monolayer was exposed to amylin-mediated stress to determine whether amylin stress downregulates LRP1, the Aβ efflux transporter. This allowed us to use pharmacology to rescue the endothelial LRP1. Results: In human AD brains, Aβ accumulation within the perivascular space frequently co-localized with deposits of amylin in the vessel wall. In rats with pancreatic expression of amyloid-forming human amylin, the high blood levels of human amylin promoted amylin deposition in brain capillaries, increased brain Aβ level, lowered plasma-to-brain Aβ ratio and suppressed expression of LRP1 protein. In vitro BBB model experiment revealed that amylin-induced stress downregulates LRP1 in endothelial cells through a miRNA-based translational repression mechanism. Conclusions: High blood human amylin levels cause cerebral microvascular dysfunction and interfere with Aβ efflux across the BBB through miRNA-mediated LRP1 downregulation. Lowering the blood amylin level in early AD could improve Aβ clearance from the brain.

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Anti-miRNA oligonucleotides: A comprehensive guide for design

Cited by 201 publications

References 138 publications

Multiple Endocrine Neoplasia Type 1: The Potential Role of microRNAs in the Management of the Syndrome

Multiple Endocrine Neoplasia Type 1: The Potential Role of microRNAs in the Management of the Syndrome

Potential miRNAs for miRNA-Based Therapeutics in Breast Cancer

Amylin-mediated regulation of LRP1 by miR-103/107 induces cerebral microvascular dysfunction and impairs β-amyloid efflux

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