The important role of miR-1-3p in cancers

Dai, Shangming; Li, Fengjiao; Xu, Shuoguo; Hu, Jinda; Gao, Lichen

doi:10.1186/s12967-023-04649-8

Cited by 6 publications

(1 citation statement)

References 194 publications

(210 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MiR-1-3p is encoded by the miR-1-2 gene located on CHR 18q11.2 ( 100 ). Wang et al found that the level of miRNA-1-3p is decreased in CMEC when chronic heart failure occurs ( 101 ).…”

Section: Role Of Mirna In Cmec In Cardiovascular Diseasementioning

confidence: 99%

Role and mechanism of miRNA in cardiac microvascular endothelial cells in cardiovascular diseases

Yan,

Zhong,

Zhao

et al. 2024

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

The occurrence and development of myocardial dysfunction are associated with damage in the cardiac microvascular endothelial cells (CMECs), which can regulate nutrient exchange and oxy-gen-carbon cycling to protect cardiomyocytes. Interventions targeting microRNAs (miRNAs) can effectively mitigate CMEC injury and thus improve cardiovascular diseases. MiRNAs are a class of noncoding single-strand RNA molecules typically 21–23 nucleotides in length that are encoded by endogenous genes. They are critical regulators of organism development, cell differentiation, metabolism, and apoptosis. Current clinical trials on miRNA drugs indicate that patient-specific miRNA levels are now being used as one of the criteria for predicting heart disease. However, the cellular process of various miRNAs in CMECs in cardiovascular diseases has not been fully elucidated. These mechanisms are a field that immediately requires further investigation. Accordingly, this review summarizes the roles and mechanisms of various miRNAs in CMECs in cardiovascular disease and includes the process of CMEC crosstalk between miRNAs and other cell types in the heart. Our study serves as a theoretical basis for the formal introduction of miRNA use into the treatment of cardiovascular diseases in the future.

show abstract

“…MiR-1-3p is encoded by the miR-1-2 gene located on CHR 18q11.2 ( 100 ). Wang et al found that the level of miRNA-1-3p is decreased in CMEC when chronic heart failure occurs ( 101 ).…”

Section: Role Of Mirna In Cmec In Cardiovascular Diseasementioning

confidence: 99%

Role and mechanism of miRNA in cardiac microvascular endothelial cells in cardiovascular diseases

Yan,

Zhong,

Zhao

et al. 2024

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

show abstract

Screening and identification of miRNAs negatively regulating FAM83A/Wnt/β-catenin signaling pathway in non-small cell lung cancer

Yuan,

Liu,

Huang

et al. 2024

Sci Rep

View full text Add to dashboard Cite

The prevalence of non-small cell lung cancer (NSCLC) accounts for 85% of all lung cancers, with the Wnt/β-catenin signaling pathway exhibiting robust activation in this particular subtype. The expression of FAM83A (family with sequence similarity 83, member A) has been found to be significantly upregulated in lung cancer, leading to the stabilization of β-catenin and activation of the Wnt signaling pathway. In this study, we conducted a screening of down-regulated miRNAs in lung cancer with FAM83A as the target. Ultimately, we identified miR-1 as a negative regulator of FAM83A and confirmed that FAM83A is a direct target gene of miR-1 through dual luciferase reporter assays. The overexpression of miR-1 significantly attenuated the expression level of FAM83A and suppressed the Wnt signaling pathway, leading to a reduction in the expression levels of downstream target genes AXIN2, CyclinD1, and C-MYC. Additionally, it decreased the nuclear translocation of β-catenin. In addition, overexpression of miR-1 accelerated the degradation of β-catenin by inhibiting FAM83A, promoted the assembly of β-catenin degradation complex, and inhibited the proliferation, migration and invasion of NSCLC cells. In summary, miR-1 may be a potential candidate miRNA for the treatment of NSCLC.

show abstract

microRNA-1 Regulates Metabolic Flexibility in Skeletal Muscle via Pyruvate Metabolism

Ismaeel,

Peck,

Montgomery

et al. 2024

Preprint

View full text Add to dashboard Cite

MicroRNA-1 (miR-1) is the most abundant miRNA in adult skeletal muscle. To determine the function of miR-1 in adult skeletal muscle, we generated an inducible, skeletal muscle-specific miR-1 knockout (KO) mouse. Integration of RNA-sequencing (RNA-seq) data from miR-1 KO muscle with Argonaute 2 enhanced crosslinking and immunoprecipitation sequencing (AGO2 eCLIP-seq) from human skeletal muscle identified miR-1 target genes involved with glycolysis and pyruvate metabolism. The loss of miR-1 in skeletal muscle induced cancer-like metabolic reprogramming, as shown by higher pyruvate kinase muscle isozyme M2 (PKM2) protein levels, which promoted glycolysis. Comprehensive bioenergetic and metabolic phenotyping combined with skeletal muscle proteomics and metabolomics further demonstrated that miR-1 KO induced metabolic inflexibility as a result of pyruvate oxidation resistance. While the genetic loss of miR-1 reduced endurance exercise performance in mice and inC. elegans,the physiological down-regulation of miR-1 expression in response to a hypertrophic stimulus in both humans and mice causes a similar metabolic reprogramming that supports muscle cell growth. Taken together, these data identify a novel post-translational mechanism of adult skeletal muscle metabolism regulation mediated by miR-1.

show abstract

The important role of miR-1-3p in cancers

Cited by 6 publications

References 194 publications

Role and mechanism of miRNA in cardiac microvascular endothelial cells in cardiovascular diseases

Role and mechanism of miRNA in cardiac microvascular endothelial cells in cardiovascular diseases

Screening and identification of miRNAs negatively regulating FAM83A/Wnt/β-catenin signaling pathway in non-small cell lung cancer

microRNA-1 Regulates Metabolic Flexibility in Skeletal Muscle via Pyruvate Metabolism

Contact Info

Product

Resources

About