miRNA-125b-5p Suppresses Hypothyroidism Development by Targeting Signal Transducer and Activator of Transcription 3

Liu, Xiu; Xing, Qinghe; Mao, Jinyuan; Sun, Huakun; Teng, Weiping; Shan, Zhongyan

doi:10.12659/msm.907510

Cited by 8 publications

(5 citation statements)

References 31 publications

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“…We predicted that STAT3 might be the target gene of miR-125b-5p through bioinformatics analysis. [40] This result suggests that STAT3 is associated with stemness, which is somewhat similar to our finding that the miR-125b-5p/STAT3 axis regulates the activity of HCC stem cells. In addition to STAT3, Smad4 is also predicted as a nonconservative target of miR-125b-5p and had been reported associating with EMT and CSC in HCC previously.…”

Section: Discussionsupporting

confidence: 89%

“…[39] Interestingly, in the neural stem cell line C17.2, miR-125b-5p promotes cell differentiation into neurons by regulating STAT3 protein expression via binding to the first site in the STAT3 3′ UTR. [40] This result suggests that STAT3 is associated with stemness, which is somewhat similar to our finding that the miR-125b-5p/STAT3 axis regulates the activity of HCC stem cells. STAT3 has been reported to be intimately associated with β-Catenin-mediated EMT potential and CSC activity in various malignancies.…”

Section: Discussionsupporting

confidence: 89%

“…In gangliocytes, miR‐125b‐5p regulation of STAT3 is related to a neuropathic pain phenotype . Interestingly, in the neural stem cell line C17.2, miR‐125b‐5p promotes cell differentiation into neurons by regulating STAT3 protein expression via binding to the first site in the STAT3 3′ UTR . This result suggests that STAT3 is associated with stemness, which is somewhat similar to our finding that the miR‐125b‐5p/STAT3 axis regulates the activity of HCC stem cells.…”

Section: Discussionsupporting

confidence: 87%

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Development of a Non‐Coding‐RNA‐based EMT/CSC Inhibitory Nanomedicine for In Vivo Treatment and Monitoring of HCC

Guo

Wang

et al. 2019

Advanced Science

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The objective of this study is to improve the overall prognosis of patients with hepatocellular carcinoma (HCC); therefore, new therapeutic methods that can be used in vivo are urgently needed. In this study, the relationship between the quantities of microRNA (miR)‐125b‐5p in clinical specimens and clinicopathological parameters is analyzed. A folate‐conjugated nanocarrier is used to transfect miR‐125b‐5p in vivo and to observe the therapeutic effect on HCC. The inhibitory effect and mechanism of miR‐125b‐5p on hepatoma cells are also studied. Data from clinical specimens and in vitro experiments confirm that the miR‐125b‐5p quantity is negatively correlated with progression, and the target protein that regulates the epithelial–mesenchymal transition (EMT)/cancer stem cells (CSC) potential in HCC is STAT3. The miR‐125b‐5p/STAT3 axis inhibits the invasion, migration, and growth of HCC via inactivation of the wnt/β‐Catenin pathway. miR‐125b‐5p‐loaded nanomedicine effectively inhibits the EMT/CSC potential of hepatoma cells in vivo together with their magnetic resonance imaging (MRI) visualization characteristics. An HCC‐therapeutic and MRI‐visible nanomedicine platform that achieves noninvasive treatment effect monitoring and timely individualized treatment course adjustment is developed.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 87%

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Development of a Non‐Coding‐RNA‐based EMT/CSC Inhibitory Nanomedicine for In Vivo Treatment and Monitoring of HCC

Guo

Wang

et al. 2019

Advanced Science

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“…348 Besides, miR-125b-5p inhibits the pathogenesis of hypothyroidism by targeting STAT3. 349 Wang et al 350 found that NEAT1 is involved in the impaired endothelial functions in subclinical hypothyroidism (SCH). NEAT1 serves as a sponge for miR-126, disinhibiting the expression of TRAF7, thus exacerbating endothelial apoptosis and impairing vascular function in patients with SCH.…”

Section: The Role Of Epigenetic Regulation In Other Metabolic Diseasesmentioning

confidence: 99%

Epigenetic regulation in metabolic diseases: mechanisms and advances in clinical study

Lin

et al. 2023

Sig Transduct Target Ther

104

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Epigenetics regulates gene expression and has been confirmed to play a critical role in a variety of metabolic diseases, such as diabetes, obesity, non-alcoholic fatty liver disease (NAFLD), osteoporosis, gout, hyperthyroidism, hypothyroidism and others. The term ‘epigenetics’ was firstly proposed in 1942 and with the development of technologies, the exploration of epigenetics has made great progresses. There are four main epigenetic mechanisms, including DNA methylation, histone modification, chromatin remodelling, and noncoding RNA (ncRNA), which exert different effects on metabolic diseases. Genetic and non-genetic factors, including ageing, diet, and exercise, interact with epigenetics and jointly affect the formation of a phenotype. Understanding epigenetics could be applied to diagnosing and treating metabolic diseases in the clinic, including epigenetic biomarkers, epigenetic drugs, and epigenetic editing. In this review, we introduce the brief history of epigenetics as well as the milestone events since the proposal of the term ‘epigenetics’. Moreover, we summarise the research methods of epigenetics and introduce four main general mechanisms of epigenetic modulation. Furthermore, we summarise epigenetic mechanisms in metabolic diseases and introduce the interaction between epigenetics and genetic or non-genetic factors. Finally, we introduce the clinical trials and applications of epigenetics in metabolic diseases.

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“…In this sense, it has been described that up-regulation of miR-125a contributed to the differentiation of monocytes towards the inflammatory phenotype [27] through the repression of the TNFAIP3 a negative regulator of NF-kB signaling [28], and that miR-125a was upregulated in oxLDL activated macrophages [29]. Lastly, members of the miR-125 family have been shown to target transcripts whose product could be also involved in mechanisms promoting ATH onset and progression, as STAT3 [30], FOXP3 [31], VEGF [32], MARK1 [33], and BCL2, BCL2L12 and MCL1 [34] among others.…”

Section: Introductionmentioning

confidence: 99%

An Exonic Switch Regulates Differential Accession of microRNAs to the Cd34 Transcript in Atherosclerosis Progression

Hueso

Cruzado

Navarro³

2019

Genes

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Background: CD34+ Endothelial Progenitor Cells (EPCs) play an important role in the recovery of injured endothelium and contribute to atherosclerosis (ATH) pathogenesis. Previously we described a potential atherogenic role for miR-125 that we aimed to confirm in this work. Methods: Microarray hybridization, TaqMan Low Density Array (TLDA) cards, qPCR, and immunohistochemistry (IHC) were used to analyze expression of the miRNAs, proteins and transcripts here studied. Results: Here we have demonstrated an increase of resident CD34-positive cells in the aortic tissue of human and mice during ATH progression, as well as the presence of clusters of CD34-positive cells in the intima and adventitia of human ATH aortas. We introduce miR-351, which share the seed sequence with miR-125, as a potential effector of CD34. We show a splicing event at an internal/cryptic splice site at exon 8 of the murine Cd34 gene (exonic-switch) that would regulate the differential accession of miRNAs (including miR-125) to the coding region or to the 3’UTR of Cd34. Conclusions: We introduce new potential mediators of ATH progression (CD34 cell-clusters, miR-351), and propose a new mechanism of miRNA action, linked to a cryptic splicing site in the target-host gene, that would regulate the differential accession of miRNAs to their cognate binding sites.

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miRNA-125b-5p Suppresses Hypothyroidism Development by Targeting Signal Transducer and Activator of Transcription 3

Cited by 8 publications

References 31 publications

Development of a Non‐Coding‐RNA‐based EMT/CSC Inhibitory Nanomedicine for In Vivo Treatment and Monitoring of HCC

Development of a Non‐Coding‐RNA‐based EMT/CSC Inhibitory Nanomedicine for In Vivo Treatment and Monitoring of HCC

Epigenetic regulation in metabolic diseases: mechanisms and advances in clinical study

An Exonic Switch Regulates Differential Accession of microRNAs to the Cd34 Transcript in Atherosclerosis Progression

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