Delving into the Latest Updates on miR-210 with Synapse

Overview

Basic Info

Drug Type

Oligonucleotide

Synonyms

MIR-210

Target

MAX x c-Myc

Action

modulators

Mechanism

MAX modulators(MYC associated factor X modulators), MYC modulators(Myc proto-oncogene protein modulators)

Therapeutic Areas

Neoplasms

Active Indication-

Inactive Indication

Neoplasms

Originator Organization

Merck & Co., Inc.

Active Organization-

Inactive Organization

Merck & Co., Inc.

License Organization-

Drug Highest PhasePendingDiscovery

First Approval Date-

Regulation-

Structure/Sequence

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Lung cancer is one of the major cancer-related deaths in the world due to the low success rate in invasive diagnostic procedures and late staging. Hypoxia-associated molecular signatures have received attention due to a growing demand for non-invasive prognostic biomarkers, and miR-210 has been repoured as the only viable candidate. Tumor hypoxia is a characteristic of highly malignant lung cancer, and hypoxia-inducible factors increase miR-210 in this process as a way of allowing cancer cells to inhabit low oxygen conditions and grow further in lung cancer. MiR-210 takes up the responsibility of angiogenesis, survival, and metastasis. Notably, miR-210 is located downstream as a non-invasive diagnostic biomarker because of its stability and measurability in biofluids, including serum and plasma. Existing techniques, which can accurately detect miR-210 employing liquid biopsy and quantitative reverse transcription polymerase chain reaction (qRT-PCR), provide sensitivity and specificity, making it possible for early detection of hypoxic cancers. In addition to diagnostics, miR-210 is a cure different from other existing treatments as they show lesser efficiency because of hypoxia-resistant genes that may be suppressed by using miR-210. While it holds great promise, such problems as biological variation and the uniformity of the detection techniques may need further research. MiR-210 holds significant possibilities in Lung cancer diagnosis and treatment; however, there is a need for further investigation and confirmation to place miR-210 in the list of biomarkers for customized medicine.

01 Jan 2025·British Journal of Pharmacology

miR‐210 as a therapeutic target in diabetes‐associated endothelial dysfunction

Article

Author: Catrina, Sergiu‐Bogdan ; Mahdi, Ali ; Zhou, Zhichao ; Zheng, Xiaowei ; Zaccagnini, Germana ; Pernow, John ; Kontidou, Eftychia ; Rethi, Bence ; Tengbom, John ; Carlström, Mattias ; Martelli, Fabio ; Alvarsson, Michael ; Chernogubova, Ekaterina ; Jiao, Tong ; Collado, Aida ; Yang, Jiangning ; Carvalho, Lucas Rannier Ribeiro Antonino ; Zhao, Allan

Abstract:

Background and Purpose:

MicroRNA (miR)‐210 function in endothelial cells and its role in diabetes‐associated endothelial dysfunction are not fully understood. We aimed to characterize the miR‐210 function in endothelial cells and study its therapeutic potential in diabetes.

Experimental Approach:

Two different diabetic mouse models (db/db and Western diet‐induced), miR‐210 knockout and transgenic mice, isolated vessels and human endothelial cells were used.

Key Results:

miR‐210 levels were lower in aortas isolated from db/db than in control mice. Endothelium‐dependent relaxation (EDR) was impaired in aortas from miR‐210 knockout mice, and this was restored by inhibiting miR‐210 downstream protein tyrosine phosphatase 1B (PTP1B), mitochondrial glycerol‐3‐phosphate dehydrogenase 2 (GPD2), and mitochondrial oxidative stress. Inhibition of these pathways also improved EDR in both diabetic mouse models. High glucose reduced miR‐210 levels in endothelial cells and impaired EDR in mouse aortas, effects that were reversed by overexpressing miR‐210. However, plasma miR‐210 levels were not affected in individuals with type 2 diabetes (T2D) following improved glycaemic status. Of note, genetic overexpression using miR‐210 transgenic mice and pharmacological overexpression using miR‐210 mimic in vivo ameliorated endothelial dysfunction in both diabetic mouse models by decreasing PTP1B, GPD2 and oxidative stress. Genetic overexpression of miR‐210 altered the aortic transcriptome, decreasing genes in pathways involved in oxidative stress. miR‐210 mimic restored decreased nitric oxide production by high glucose in endothelial cells.

Conclusion and Implications:

This study unravels the mechanisms by which down‐regulated miR‐210 by high glucose induces endothelial dysfunction in T2D and demonstrates that miR‐210 serves as a novel therapeutic target.

LINKED ARTICLES:

This article is part of a themed issue Non‐coding RNA Therapeutics. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v182.2/issuetoc

30 Oct 2023·Journal of orthopaedic surgery and research

MiR-210 promotes bone formation in ovariectomized rats by regulating osteogenic/adipogenic differentiation of bone marrow mesenchymal stem cells through downregulation of EPHA2.

Article

Author: Lv, Xiangyu ; Tan, Jiuting ; Ren, Lijue ; Wang, Jiahui ; Zhu, Xiaohui ; Hua, Fei

PURPOSE:

In osteoporosis, the balance between osteogenic and adipogenic differentiation of mesenchymal stem cells (MSCs) is disrupted. The osteogenic differentiation of bone marrow MSCs (BMSCs) is important for improving osteoporosis. The aim of this study was to explore the role and molecular mechanism of miR-210 in the balance of osteogenic/adipogenic differentiation of BMSCs in postmenopausal osteoporosis.

METHODS:

Postmenopausal osteoporosis rat models were constructed by ovariectomy (OVX). BMSCs were isolated from the femur in rats of Sham and OVX groups. MiR-210 was overexpressed and suppressed by miR-210 mimics and inhibitor, respectively. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the relative mRNA expression of miR-210, ephrin type-A receptor 2 (EPHA2), alkaline phosphatase (ALP), osterix (OSX), osteocalcin (Bglap), Runt-related transcription factor 2 (Runx2), peroxisome proliferator activated receptor gamma, and fatty acid binding protein 4 (FABP4) in each group of rat femoral tissues or BMSCs. Western blot was applied to detect the protein expression level of EPHA2 in rat femoral tissues and cells. Alizarin red S staining and oil red O staining were performed to assess the osteogenic and adipogenic differentiation of BMSCs, respectively. In addition, the targeting relationship between miR-210 and EPHA2 was verified by a dual luciferase gene reporter assay.

RESULTS:

The expression of miR-210 was significantly reduced in femoral tissues and BMSCs of OVX rats, and its low expression was associated with reduced bone formation. The osteogenic differentiation was enhanced in OVX rats treated with miR-210 mimic. Overexpression of miR-210 in transfected BMSCs was also found to significantly promote osteogenic differentiation and even inhibit adipogenic differentiation in BMSCs, while knockdown of miR-210 did the opposite. Further mechanistic studies showed that miR-210 could target and inhibit the expression of EPHA2 in BMSCs, thus promoting osteogenic differentiation and inhibiting adipogenic differentiation of BMSCs.

CONCLUSION:

MiR-210 promotes osteogenic differentiation and inhibits adipogenic differentiation of BMSCs by down-regulating EPHA2 expression. As it plays an important role in the osteogenic/adipogenic differentiation of osteoporosis, miR-210 can serve as a potential miRNA biomarker for osteoporosis.

100 Deals associated with miR-210

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