Reductions in the expression of miR-124-3p, miR-128-1, and miR-221-3p in pediatric astrocytomas are related to high-grade supratentorial, and recurrent tumors in Mexican children

Eguía-Aguilar, Pilar; Pérezpeña-Díazconti, Mario; Benadón-Darszon, Eduardo; León, Fernando Chico-Ponce de; Gordillo-Domínguez, Luis Felipe; Torres-García, Samuel; Sadowinski-Pine, Stanislaw; Arenas-Huertero, Francisco

doi:10.1007/s00381-014-2416-5

Cited by 14 publications

(8 citation statements)

References 32 publications

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“…Therefore, our finding of its involvement in CAD may provide novel evidence for deeper research in this area. MiR‐221‐3p was identified as a novel marker for an early prediction of acute myocardial infarction (AMI) in earlier reports, and the increased expression levels of this miRNA was also found in AMI patients, which was consistent with the finding in this study of its upregulation in CAD patients. Besides, it was found that the miRNA, which was previously upregulated, was significantly downregulated after the treatment of CAD patients.…”

Section: Discussionsupporting

confidence: 91%

Identification of six miRNAs serving as predictive biomarkers in coronary artery disease

Ren

Gao²,

Ke³

et al. 2018

J of Cellular Biochemistry

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Coronary artery disease (CAD) is quite a common disease with high risk. It was reported that microRNAs (miRNAs) had significant effect on the occurrence of CAD. The previously published results are inconsistent due to the parameters, such as sequencing platform, samples selection, and the filter conditions. Here we aimed to explore the critical miRNAs in the occurrence of CAD, which may function as the potential biomarkers. A total of 12 representative datasets of miRNAs related to the occurrence of miRNAs were finally selected, and the critical miRNAs were determined by the comparison of the overlap relations. TargetScan software was used to predict the target genes of these critical miRNAs. Besides, DAVID and Tfacts dataset were used to analyze the functional enrichment and the transcriptional factors analysis. At last, a total of six signature miRNAs were identified, among which five were significantly upregulated and one was downregulated. The target gene of upregulated miRNAs was mostly enriched in the process of RNA Polymerase II promoter and the transcription of DNA template, whereas the target genes of downregulated miRNAs were mostly enriched in the regulation of transcription, DNA‐templated. Besides, the result of the transcriptional factor analysis showed that there were 43 factors coexisting in two kinds of target genes. In summary, six critical miRNAs, as well as the corresponding target genes and transcriptional factors, were identified in the occurrence of CAD by bioinformatics analysis. These identified miRNAs may function as potential biomarkers in the clinical management of CAD.

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Section: Discussionsupporting

confidence: 91%

Identification of six miRNAs serving as predictive biomarkers in coronary artery disease

Ren

Gao²,

Ke³

et al. 2018

J of Cellular Biochemistry

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“…The antitumor effect of miR‐124‐3p in GBM cells is enhanced through gap junctions by partly decreasing CDK6 expression . Furthermore, miR‐124‐3p is associated with malignant tumor progression and poor prognosis in glioma patients and is related to recurrent high‐grade gliomas in Mexican children, indicating that miR‐124‐3p is a potential biomarker for glioma. Therefore, one miRNA can target multiple genes and affect various cellular pathways, and this study clearly showed that PIM1 is also a direct target gene of miR‐124‐3p.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐124‐3p regulates cell proliferation, invasion, apoptosis, and bioenergetics by targeting PIM1 in astrocytoma

Deng

Wang

Yao³

et al. 2016

Cancer Science

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The PIM1 protein is an important regulator of cell proliferation, the cell cycle, apoptosis, and metabolism in various human cancers. MicroRNAs (miRNAs) are powerful post‐transcriptional gene regulators that function through translational repression or transcript destabilization. Therefore, we aimed to identify whether a close relationship exists between PIM1 and miRNAs. PIM1 protein levels and mRNA levels were significantly upregulated in astrocytoma tissues, indicating the oncogenic role of PIM1 in astrocytoma. Further bioinformatics analysis indicated that miR‐124‐3p targeted the 3′‐UTR of PIM1. We also observed an inverse correlation between the miR‐124‐3p levels and PIM1 protein or mRNA levels in astrocytoma samples. Next, we experimentally confirmed that miR‐124‐3p directly recognizes the 3′‐UTR of the PIM1 transcript and regulates PIM1 expression at both the protein and mRNA levels. Furthermore, we examined the biological consequences of miR‐124‐3p targeting PIM1 in vitro. We showed that the repression of PIM1 in astrocytoma cancer cells by miR‐124‐3p suppressed proliferation, invasion, and aerobic glycolysis and promoted apoptosis. We observed that the restoration or inhibition of PIM1 activity resulted in effects that were similar to those induced by miR‐124‐3p inhibitors or mimics in cancer cells. Finally, overexpression of PIM1 rescued the inhibitory effects of miR‐124‐3p. In summary, these findings aid in understanding the tumor‐suppressive role of miR‐124‐3p in astrocytoma pathogenesis through the inhibition of PIM1 translation.

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“…MiR-124-3p has been confirmed to be downregulated in glioma tissues, and loss of miR-124-3p is associated with high malignance and poor prognosis in patients with glioma [31, 32]. Furthermore, the relative levels of miR-124-3p in serum exosomes could serve as a complementary diagnostic biomarker, providing a minimally invasive and innovative tool to diagnose gliomas at their onset and predict metastases and glioma grading before surgery [33].…”

Section: Discussionmentioning

confidence: 99%

p62 acts as an oncogene and is targeted by miR-124-3p in glioma

et al. 2019

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BackgroundGlioma is the most common central nervous system (CNS) tumour. p62, an important autophagy adaptor, plays a crucial role in cancer. However, the role of p62 in the progression of glioma is poorly characterized.MethodsWe examined the expression of p62 in glioma tissues and cell lines. Then we investigated the function of p62 in vitro, and clarified the mechanism underlying the regulation of p62 expression.ResultsWe revealed that p62 was upregulated at both the mRNA and protein levels in human glioma tissues irrelevant to isocitrate dehydrogenase (IDH) status. Then, we found that overexpression of p62 promoted glioma progression by promoting proliferation, migration, glycolysis, temozolomide (TMZ) resistance and nuclear factor κB (NF-κB) signalling pathway, and repressing autophagic flux and reactive oxygen species (ROS) in vitro. In accordance with p62 overexpression, knockdown of p62 exerted anti-tumour effects in glioma cells. Subsequently, we demonstrated that miR-124-3p directly targeted the 3′-UTR of p62 mRNA, leading to the downregulation of p62. Finally, we found that p62 function could be partially reversed by miR-124-3p overexpression.ConclusionsOur results demonstrate that p62 can be targeted by miR-124-3p and acts as an oncogene in glioma, suggesting the potential value of p62 as a novel therapeutic target for glioma.

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Reductions in the expression of miR-124-3p, miR-128-1, and miR-221-3p in pediatric astrocytomas are related to high-grade supratentorial, and recurrent tumors in Mexican children

Abstract: The low expression of these miRNAs may constitute a potential marker of astrocytomas that correlates with localization, possibly due to alterations in the maturation processes of these miRNAs that produced low mature forms in patients with recurrent pediatric astrocytomas.

Cited by 14 publications

References 32 publications

Identification of six miRNAs serving as predictive biomarkers in coronary artery disease

Identification of six miRNAs serving as predictive biomarkers in coronary artery disease

MicroRNA‐124‐3p regulates cell proliferation, invasion, apoptosis, and bioenergetics by targeting PIM1 in astrocytoma

p62 acts as an oncogene and is targeted by miR-124-3p in glioma

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