Alteration in microRNA‐17‐92 dynamics accounts for differential nature of cellular proliferation

Sengupta, Debapriya; Govindaraj, Vinodhini; Kar, Sandip

doi:10.1002/1873-3468.12974

Cited by 12 publications

(27 citation statements)

References 62 publications

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“…MiR-19b is an important part of miR-17/92 cluster and decreased expression of miR-19b may cause the defect of ventricular septal and short life span in mice. 7 Moreover, it was reported as an antithrombotic factor in IHD patients and a potential biomarker of human cell ageing. 8,9 Previous study also indicated that miR-19b attenuate endothelial cell apoptosis which is induced by tumour necrosis factor-α (TNF-α) and play role in cardiac fibroblast proliferation.…”

Section: Introductionmentioning

confidence: 99%

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Diagnostic value of circulating microRNA‐19b in heart failure

Zhang

Liu

et al. 2020

Eur J Clin Investigation

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Objective: For differentiating heart failure (HF) with preserved ejection fraction (HFpEF) from HF with reduced EF (HFrEF), N-terminal prohormone brain natriuretic peptide (NT-proBNP) is less accurate. Decreased expression of microRNA-19b (miR-19b) is associated with increased cardiac-fibrosis. We aim to evaluate the value of miR-19b in diagnosing HFrEF patients. Method: We included 200 HF patients and 100 healthy controls. Intergroup comparisons of miR-19b were made and correlation between miR-19b and NT-proBNP was analysed. Diagnostic values of NT-proBNP and miR-19b for HF patients versus controls and HFrEF versus HFpEF were obtained by ROC analysis and described by area under curve (AUC), sensitivity and specificity. Results: HFrEF patients (0.87, 95% CI 0.37-1.45) had significantly lower miR-19b level than HFpEF group (1.32, 95% CI 0.63-2.51) and the controls (1.82, 95% CI 0.37-1.45) (both P < .001). There was a remarkable negative correlation between miR-19b and NT-proBNP (P < .001). The additional use of miR-19b did not improve the accuracy of NT-proBNP alone in diagnosing HF patients from the controls (both AUC = 0.98, 95%CI 0.97-0.99). However, as for distinguishing the HFpEF from HFrEF, miR-19b and NT-proBNP yielded a significantly higher AUC than NT-proBNP alone (0.85, 95% CI 0.80-0.90 vs. 0.66, 95% CI 0.58-0.74) (P < .001), and the sensitivity for diagnosing HFrEF was raised from 58% to 77% and the specificity from 75% to 79%. Conclusions: On top of NT-proBNP, miR-19b added the value in diagnosing HFrEF. But in view of satisfactory accuracy of NT-proBNP in predicting HF from the healthy volunteers, miR-19b did not provide incremental value.

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Section: Introductionmentioning

confidence: 99%

“…MiR‐19b is an important part of miR‐17/92 cluster and decreased expression of miR‐19b may cause the defect of ventricular septal and short life span in mice 7 . Moreover, it was reported as an antithrombotic factor in IHD patients and a potential biomarker of human cell ageing 8,9 .…”

Section: Introductionmentioning

confidence: 99%

Diagnostic value of circulating microRNA‐19b in heart failure

Zhang

Liu

et al. 2020

Eur J Clin Investigation

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“…MiRs have been exquisitely described to control gene expression by binding to mRNA targets using the seed sequences, and miRs with the same or similar seed sequences and origin are grouped into one family or cluster [ 15 ]. The miR-17 family consists of the miR-17-92 cluster, miR-106a-363 cluster and miR-106b-25 cluster [ 17 ], and the miR-17 family has been well documented to influence the survival, differentiation and functions of various kinds of mammalian cells [ 18 , 19 ]. However, the effects of miRs associated with the miR-17 family in myogenesis are controversial.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-106a-5p Inhibited C2C12 Myogenesis via Targeting PIK3R1 and Modulating the PI3K/AKT Signaling

Zhu

Zhang

et al. 2018

Genes

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The microRNA (miR)-17 family is widely expressed in mammalian tissues and play important roles in various physiological and pathological processes. Here, the functions of miR-106a-5p, a member of miR-17 family, were explored during myogenic differentiation in C2C12 cell line. First, miR-106a-5p was found to be relatively lower expressed in two-month skeletal muscle tissues and gradually decreased upon myogenic stimuli. Forced expression of miR-106a-5p significantly reduced the differentiation index, fusion index as well as the expression of myogenic markers (MyoD, MyoG, MyHC, Myomixer, Myomarker). Meanwhile, the levels of phosphorylated AKT were reduced by overexpression of miR-106a-5p, and administration of insulin-like growth factor 1 (IGF1), a booster of myogenic differentiation, could recover all the inhibitory effects above of miR-106a-5p. Furthermore, miR-106a-5p was elevated in aged muscles and dexamethasone (DEX)-treated myotubes, and up-regulation of miR-106a-5p significantly reduced the diameters of myotubes accompanied with increased levels of muscular atrophy genes and decreased PI3K/AKT activities. Finally, miR-106a-5p was demonstrated to directly bind to the 3’-UTR of PIK3R1, thus, repress the PI3K/AKT signaling.

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“…MiR-7153-5p shares the 7-nt seed sequence with miR-146a-5p, which belongs to the miR-146 family, known to be involved in the inhibition of macrophage-induced apoptosis, angiogenesis activation [26], and metastasis formation in renal cell cancer [27]. And miR-106b-5p shares the 7-nt seed sequence with miR-17-5p, which belongs to the miR-17-92 cluster family, and is implicated in a wide variety of malignancies [28]; for example, miR-106b-5p activates cell proliferation and inhibits apoptosis in non-small cell lung cancer [29].…”

Section: Discussionmentioning

confidence: 99%

Detection of a MicroRNA molecular signature of ultraviolet radiation in the superficial regions of melanocytic nevi on sun-exposed skin

Bell

Chakravarti

et al. 2018

Modern Pathology

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How melanocytes transform into melanoma cells remains largely unknown. However, prolonged ultraviolet radiation exposure is linked with melanoma, and the DNA of melanomas arising in chronically sun-exposed skin is characterized by an elevated number of pyrimidine transitions, mainly C>T (predominantly caused by ultraviolet B), and transversions of GC>TA or AT>CG (caused by ultraviolet A over indirect mechanisms). Since ultraviolet penetrates mostly only the superficial dermis, we sought to determine the extent to which superficial and deep melanocytes of nevi in sun-exposed skin differ in their miRNA expression and consider the changes as likely secondary to ultraviolet radiation-induced damage. The differentially expressed miRNAs were analyzed for known potential oncomiRs or linked to potential oncogenes or tumor suppressors. Superficial and deep melanocytes were microdissected from the nevi of 14 patients. The suspensions were processed for hybridization to a ribonucleotide protection system with 2280 total probes, including 2256 miRNA probes targeting 2083 human miRNAs. A comprehensive analysis of all human miRNAs registered in miRBase 11.0 was performed using the HTG Molecular Diagnostic database. Statistical analysis of these data yielded for 14 samples a statistically relevant profile of 39 miRNA species at FDR<0.1 that were differentially expressed between superficial and deep melanocytes. Ingenuity Pathway Analysis based on the expression data of these 39 miRNAs suggested the gene transcripts AR, MDM2, SMAD2/3, and YBX1 as the most probable miRNA targets, which were validated at the protein level. Our findings suggest that superficial ultraviolet radiation-damaged melanocytes can be differentiated from deep melanocytes on the basis of the expression of 39 miRNAs, the most probable gene transcript and protein targets of which are AR, MDM2, SMAD2/3, and YBX1, with YBX1 expression validating the best the molecular signature in immunohistochemical analysis.

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Alteration in microRNA‐17‐92 dynamics accounts for differential nature of cellular proliferation

Cited by 12 publications

References 62 publications

Diagnostic value of circulating microRNA‐19b in heart failure

Diagnostic value of circulating microRNA‐19b in heart failure

MicroRNA-106a-5p Inhibited C2C12 Myogenesis via Targeting PIK3R1 and Modulating the PI3K/AKT Signaling

Detection of a MicroRNA molecular signature of ultraviolet radiation in the superficial regions of melanocytic nevi on sun-exposed skin

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