Last update 01 Nov 2024

miR-126

Last update 01 Nov 2024

Basic Info

Synonyms

hsa-mir-126, microRNA 126, MIR126

+ [1]

Introduction-

Drugs associated with miR-126

Miristen

Target

miR-126

Mechanism

miR-126 antagonists

Active Org.

City of Hope National Medical Center

Originator Org.

City of Hope National Medical Center

Active Indication

Adult Acute Myeloblastic Leukemia [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

MiR126-targeted-nanoparticles (Istituto superiore di sanità)

Target

miR-126

Mechanism

miR-126 antagonists

Active Org.

Istituto Superiore di Sanità

Originator Org.

Istituto Superiore di Sanità

Active Indication

Melanoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with miR-126

100 Translational Medicine associated with miR-126

0 Patents (Medical) associated with miR-126

2,080

Literatures (Medical) associated with miR-126

31 Dec 2024·Epigenetics

Maternal glucose levels and late pregnancy circulating extracellular vesicle and particle miRNAs in the MADRES pregnancy cohort

Article

Author: Foley, Helen B. ; Breton, Carrie V. ; Farzan, Shohreh F. ; Romano, Megan E. ; Howe, Caitlin G. ; Maldonado, Luis E. ; Gui, Jiang ; Bentz, Jessica L. ; Marsit, Carmen J. ; Levy, Joshua J. ; Bastain, Theresa M. ; Anderson, Elizabeth C.

Maternal hyperglycemia during pregnancy adversely affects maternal and child outcomes. While mechanisms are not fully understood, maternal circulating miRNAs may play a role. We examined whether continuous glucose levels and hyperglycemia subtypes (gestational diabetes, type 2 diabetes, and glucose intolerance) were associated with circulating miRNAs during late pregnancy. Seven miRNAs (hsa-miR-107, hsa-let-7b-5p, hsa-miR-126-3p, hsa-miR-181a-5p, hsa-miR-374a-5p, hsa-miR-382-5p, and hsa-miR-337-5p) were associated (p < 0.05) with either hyperglycemia or continuous glucose levels prior to multiple testing correction. These miRNAs target genes involved in pathways relevant to maternal and child health, including insulin signaling, placental development, energy balance, and appetite regulation.

01 Dec 2024·Current Cancer Drug Targets

H3K27ac-activated LncRNA NUTM2A-AS1 Facilitated the Progression of Colorectal Cancer Cells via MicroRNA-126-5p/FAM3C Axis

Article

Author: Li, Songyan ; Lin, Haiguan ; Hu, Shidong ; Teng, Da ; Li, Yuxuan ; Liu, Boyan ; Du, Xiaohui ; Yang, Yan

Objective:Long non-coding RNAs (lncRNAs) are of great importance in the process of colorectal cancer (CRC) tumorigenesis and progression. However, the functions and underlying molecular mechanisms of the majority of lncRNAs in CRC still lack clarity.Methods:A Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect lncRNA NUTM2A-AS1 expression in CRC cell lines. Cell counting kit 8 (CCK-8) assay and flow cytometry were used to examine the biological functions of lncRNA NUTM2A-AS1 in the proliferation and apoptosis of CRC cells. RT-qPCR and western blot were implemented for the detection of cell proliferation-, apoptosis-related proteins, and FAM3C. Bioinformatics analysis and dual- luciferase reporter assays were utilized to identify the mutual regulatory mechanism of ceRNAs.Results:lncRNA NUTM2A-AS1 notably elevated in CRC cell lines and the silencing of NUTM2A- AS1 declined proliferation and facilitated apoptosis. Mechanistically, NUTM2A-AS1 was transcriptionally activated by histone H3 on lysine 27 acetylation (H3K27ac) enriched at its promoter region, and NUTM2A-AS1 acted as a sponge for miR-126-5p, leading to the upregulation of FAM3C expression in CRC cell lines.Conclusion:Our research proposed NUTM2A-AS1 as an oncogenic lncRNA that facilitates CRC malignancy by upregulating FAM3C expression, which might provide new insight and a promising therapeutic target for the diagnosis and treatment of CRC.

01 Dec 2024·Molecular Biology Reports

Up-regulation of miR-126 via DNA methylation in hypoxia-preconditioned endothelial cells may contribute to hypoxic tolerance of neuronal cells

Article

Author: Gong, Kerui ; Zhang, Chunyang ; Sun, Kai ; Zhao, Zhujun ; Han, Ruijuan ; Shao, Guo ; Xu, Wenqing ; Fu, Gang ; Zhang, Pu

BACKGROUNDEndothelial cells (ECs) can confer neuroprotection by secreting molecules. This study aimed to investigate whether DNA methylation contributes to the neuroprotective gene expression induced by hypoxia preconditioning (HPC) in ECs and to clarify that the secretion of molecules from HPC ECs may be one of the molecular mechanisms of neuroprotection.METHODSHuman microvascular endothelial cell-1 (HMEC-1) was cultured under normal conditions (C), hypoxia(H), and hypoxia preconditioning (HPC), followed by the isolation of culture medium (CM). SY5Y cell incubated with the isolated CM from HMEC-1 was exposed to oxygen-glucose deprivation (OGD). The DNA methyltransferases (DNMTs), global methylation level, miR-126 and its promotor DNA methylation level in HMEC-1 were measured. The cell viability and cell injury in SY5Y were detected.RESULTSHPC decreased DNMTs level and global methylation level as well as increased miR-126 expression in HMEC-1. CM from HPC treated HMEC-1 also relieved SY5Y cell damage, while CM from HMEC-1 which over-expression of miR-126 can reduce injury in SY5Y under OGD condition.CONCLUSIONSThese findings indicate EC may secrete molecules, such as miR-126, to execute neuroprotection induced by HPC through regulating the expression of DNMTs.

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miR-126

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