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Last update 23 Jan 2025

MIR133

Last update 23 Jan 2025

Basic Info

Synonyms

miR-133 family

Introduction-

Drugs associated with MIR133

JN-210

Target

MIR133

Mechanism

MIR133 inhibitors

Active Org.

Jaan Biotherapeutics LLC

Originator Org.

Jaan Biotherapeutics LLC

Active Indication

Cardiomyopathy, Hypertrophic, Familial

Inactive Indication-

Drug Highest PhaseEarly Phase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MIR133

100 Translational Medicine associated with MIR133

0 Patents (Medical) associated with MIR133

858

Literatures (Medical) associated with MIR133

01 Jan 2025·Journal of Cellular Physiology

RETRACTION: MiR‐145 Promotes MiR‐133b Expression Through c‐myc and DNMT3A‐mediated Methylation in Ovarian Cancer Cells

RETRACTION: J. Li, S. Zhang, Y. Zou, L. Wu, M. Pei, and Y. Jiang, “MiR‐145 Promotes MiR‐133b Expression Through c‐myc and DNMT3A‐mediated Methylation in Ovarian Cancer Cells,” Journal of Cellular Physiology 235, no. 5 (2020): 4291‐4301, https://doi.org/10.1002/jcp.29306.The above article, published online on 14 October 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor‐in‐Chief, Roberth Heath; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, instances of duplicated image elements were identified in Figures 2 d, 3 d, and 5 g. Therefore, the article is retracted as the editors consider its conclusions to be invalid. The authors have been informed of the decision of retraction.

31 Dec 2024·Annals of Medicine

Combined miRNA transcriptome and proteome analysis of extracellular vesicles in urine and blood from the Pompe mouse model

Article

Author: Melber, Andrew ; Moore, Simon W. ; Li, Bin ; Su, Zhenqiang ; Moreland, Rodney ; Palmieri, Kathleen ; Merberg, David ; Makhija, Mahindra ; Carey, Galen ; Crooker, Bob ; Boyanapalli, Ruby

INTRODUCTIONAcid α-glucosidase (GAA) is a lysosomal enzyme that hydrolyzes glycogen to glucose. Deficiency of GAA causes Pompe disease (PD), also known as glycogen storage disease type II. The resulting glycogen accumulation causes a spectrum of disease severity ranging from infantile-onset PD to adult-onset PD. Additional non-invasive biomarkers of disease severity are needed to monitor response to therapeutic interventions.METHODSWe measured protein and miRNA abundance in exosomes from serum and urine from the PD mouse model (B6;129-GaaTm1Rabn/J), wild-type mice, and PD mice treated with a candidate gene therapy.RESULTSThere were significant differences in the abundance of 113 miRNA in serum exosomes from Pompe versus healthy mice. Levels of miR-206, miR-133, miR-1a, miR-486, and other important regulators of muscle development and maintenance were altered in the Pompe samples. The serum and urine exosome proteomes of healthy and Pompe mice also differed broadly. Several of the dysregulated proteins are encoded by genes with potential target sites for affected miRNA.CONCLUSIONExosomes derived from urine or serum are a potential source of biomarkers for Pompe Disease. Further study of the differences in the miRNA transcriptome and proteome content of exosomes may yield new insights into disease mechanisms.

01 Dec 2024·Cytotechnology

MiR-133 promotes the multidrug resistance of acute myeloid leukemia cells (HL-60/ADR) to daunorubicin

Article

Author: Wei, Yueping ; Tao, Wei ; Yu, Jingxing ; Yu, Kun ; Liu, Lin

This study aimed to explore the role and molecular mechanism of miR-133 in multidrug resistance in acute myeloid leukemia (AML) and provide a new theoretical basis for the treatment and prognosis of AML patients. We performed experiments at the cellular level. RT‒qPCR and Western blotting were used to detect gene and protein expression; cell viability was measured with CCK-8 assays; apoptosis was detected via flow cytometry; and a dual-luciferase reporter gene assay was used to verify the binding between miR-133 and CXCL12. In this study, we found that miR-133 was upregulated in HL-60/ADR multidrug-resistant cells. Functionally, the inhibition of miR-133 alleviated the resistance of HL-60/ADR cells to daunorubicin (DNR). After inhibiting miR-133 in HL-60/ADR cells treated with DNR, the expression of the intracellular drug resistance-related proteins MRP562 and P-gp was inhibited, cell proliferation decreased, and apoptosis increased. Mechanistically, the NF-κB signaling pathway regulates the expression of miR-133 in HL-60/ADR cells, and the targeting of CXCL12 by miR-133 enhances the resistance of HL-60/ADR cells to DNR. In conclusion, the NF-κB signaling pathway regulates the expression of miR-133, and inhibiting miR-133 expression can target CXCL12 to increase the sensitivity of HL-60/ADR cells to DNR.

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MIR133

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