Receiver operating characteristic (ROC) curve analysis revealed an area under the curve (AUC) of 0.951, with a sensitivity of 90.1% and specificity of 87.8%. These aberrantly expressed miRNAs delivered by sEVs potentially contribute to HCC pathology and may serve as diagnostic biomarkers for HCC.
In conclusion, inhibition of VEGFR2 expression in tumour cells promotes the expression of miR-3200-3p in exosomes secreted by tumour cells. miR-3200-3p enters the TME through exosomes and acts on DDB1 in Treg cells to promote senescence of Treg cells to inhibit tumour progression.
2 years ago
Journal
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CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • GSTP1 (Glutathione S-transferase pi 1) • DDB1 (Damage Specific DNA Binding Protein 1) • MIR3200 (MicroRNA 3200) • MMP3 (Matrix metallopeptidase 3)
Furthermore, our results suggest that miR-3200 enhances expression of RAB7A, and then Rab7A regulates the carcinogenic function of miR-3200 by increasing telomere remodeling in human liver cancer. These results are of great significance for the prevention and treatment of human liver cancer.
In summary, we devoted to analyzing CNV-related lncRNAs, mRNAs, and miRNAs in LUSC, thus clarifying 5 lncRNAs that may influence the malignant progression of LUSC. The ceRNA network regulated by these lncRNAs may be the novel pathogenesis of LUSC.
HULC was found to function as a ceRNA of miR-3200-5p, and miR-3200-5p regulates ferroptosis by targeting ATF4, resulting in the inhibition of proliferation and metastasis within HCC cells. In summary, these findings illuminate some of the molecular mechanisms through which downregulation of HULC induces liver cancer cell ferroptosis by targeting the miR-3200-5p/ATF4 axis to modulate the development of hepatocellular carcinoma.
Importantly, these results further showed that miR-3200-3p downregulated the proliferation and metastasis by suppressing the expression of CAMK2A, thus regulating the Ras/Raf/MEK/ERK pathway. This study provided provided insights into the biological role of miR-3200-3p, which might function as a potential biomarker in glioma therapy.
almost 4 years ago
Preclinical • Journal
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MIR3200 (MicroRNA 3200) • MIR320A (MicroRNA 320a) • CAMK2A (Calcium/Calmodulin Dependent Protein Kinase II Alpha)
miR-3200-5p exerted tumor-suppressive effects in HCC and inactivated CKAP2 and FAK-ERK pathway. All in all, this study corroborates that DARS-AS1 facilitates HCC proliferation and metastasis by regulating miR-3200-5p-mediated CKAP2, which provides a potential target for HCC diagnosis and treatment.
This circRNA can regulate activity of Notch, Wnt/β-Catenin, TGF-β/Smad, JAK1/STAT3 and AMPK signaling pathways. In the current study, we review the literature on the role of circMTO1 in the tumorigenesis.
We propose a risk score based on miR-3200-3p and miR-3690 that may be useful as a prognostic marker to predict HCC recurrence after LT. We generated a ceRNA network involving these miRNAs, which may help reveal their regulatory roles in HCC.
LogFCs in the expression of miRNAs and mRNAs from plasma exosomes after CCRT are associated with EP and metastasis, reflecting unresolved inflammation and systemic microenvironmental factors, respectively. However, this study, supported by preliminary data insufficient to reach clear conclusions, should be verified in larger prospective cohorts.
over 4 years ago
Clinical • Journal
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FCGR1A (Fc Fragment Of IgG Receptor Ia) • MIR3200 (MicroRNA 3200)
Unfortunately, differential expression of only hsa-miR-185-5p was confirmed in the validation cohort, with AUG at 0.654. Differences in miRNAs expression profiles in invasive and noninvasive gonadotropic PitNETs are slight and the level of miRNA expression seems not to be applicable as useful classifier of tumor invasiveness.
Furthermore, silencing of LINC00324 reversed the promoting effects of BCAT1 on the proliferation, migration, and invasion of GC cells. Silencing of LINC00324 inhibited the proliferation, migration, and invasion of GC cells through regulating the miR-3200-5p/BCAT1 axis.