miRNA-Dependent Activation of mRNA Translation

Ni, Wenjuan; Leng, Xiao-Min

doi:10.2174/2211536605666160825151201

Cited by 58 publications

(32 citation statements)

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“…As a result, increases in iNOS protein lead to caspase-3 activation and subsequent apoptosis [ 8 ]. CI increases not only miR-15, miR-99, and miR-100 that target IL-6 and TNF, but also let-7g and miR-98 that target STAT3, whose activation transcribes iNOS [ 61 – 64 ]. The illustration provides insight and perspective for further studies and future validation.…”

Section: Discussionmentioning

confidence: 99%

Hemorrhage enhances cytokine, complement component 3, and caspase-3, and regulates microRNAs associated with intestinal damage after whole-body gamma-irradiation in combined injury

et al. 2017

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Hemorrhage following whole-body γ-irradiation in a combined injury (CI) model increases mortality compared to whole-body γ-irradiation alone (RI). The decreased survival in CI is accompanied by increased bone marrow injury, decreased hematocrit, and alterations of miRNA in the kidney. In this study, our aim was to examine cytokine homeostasis, susceptibility to systemic bacterial infection, and intestinal injury. More specifically, we evaluated the interleukin-6 (IL-6)-induced stress proteins including C-reactive protein (CRP), complement 3 (C3), Flt-3 ligand, and corticosterone. CD2F1 male mice received 8.75 Gy 60Co gamma photons (0.6 Gy/min, bilateral) which was followed by a hemorrhage of 20% of the blood volume. In serum, RI caused an increase of IL-1, IL-2, IL-3, IL-5, IL-6, IL-12, IL-13, IL-15, IL-17A, IL-18, G-CSF, CM-CSF, eotaxin, IFN-γ, MCP-1, MIP, RANTES, and TNF-α, which were all increased by hemorrhage alone, except IL-9, IL-17A, and MCP-1. Nevertheless, CI further elevated RI-induced increases of these cytokines except for G-CSF, IFN- γ and RANTES in serum. In the ileum, hemorrhage in the CI model significantly enhanced RI-induced IL-1β, IL-3, IL-6, IL-10, IL-12p70, IL-13, IL-18, and TNF-α concentrations. In addition, Proteus mirabilis Gram(-) was found in only 1 of 6 surviving RI mice on Day 15, whereas Streptococcus sanguinis Gram(+) and Sphingomonas paucimobilis Gram(-) were detected in 2 of 3 surviving CI mice (with 3 CI mice diseased due to inflammation and infection before day 15) at the same time point. Hemorrhage in the CI model enhanced the RI-induced increases in C3 and decreases in CRP concentrations. However, hemorrhage alone did not alter the basal levels, but hemorrhage in the CI model displayed similar increases in Flt-3 ligand levels as RI did. Hemorrhage alone altered the basal levels of corticosterone early after injury, which then returned to the baseline, but in RI mice and CI mice the increased corticosterone concentration remained elevated throughout the 15 day study. CI increased 8 miRNAs and decreased 10 miRNAs in serum, and increased 16 miRNA and decreased 6 miRNAs in ileum tissue. Among the altered miRNAs, CI increased miR-34 in the serum and ileum which targeted an increased phosphorylation of ERK, p38, and increased NF-κB, thereby leading to increased iNOS expression and activation of caspase-3 in the ileum. Further, let-7g/miR-98 targeted the increased phosphorylation of STAT3 in the ileum, which is known to bind to the iNOS gene. These changes may correlate with cell death in the ileum of CI mice. The histopathology displayed blunted villi and villus edema in RI and CI mice. Based on the in silico analysis, miR-15, miR-99, and miR-100 were predicted to regulate IL-6 and TNF. These results suggest that CI-induced alterations of cytokines/chemokines, CRP, and C3 cause a homeostatic imbalance and may contribute to the pathophysiology of the gastrointestinal injury. Inhibitory intervention in these responses may prove therapeutic for CI and improve recovery of the ileal morp...

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Section: Discussionmentioning

confidence: 99%

Hemorrhage enhances cytokine, complement component 3, and caspase-3, and regulates microRNAs associated with intestinal damage after whole-body gamma-irradiation in combined injury

et al. 2017

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“…In human cancers, miRNAs are considered as mRNA sponges to mediate gene expression by binding to 3ʹ untranslated region (UTR) of downstream genes. 47 Using website microT-CDS, we found that ELF2likely bound to miR-188, and then confirmed this interaction using the dual luciferase reporter assay and RIP assay. Moreover, the negative effect of miR-188 on ELF2 expression was observed in NPC cells in this assay.…”

Section: Discussionmentioning

confidence: 68%

<p>CircRNA ZNF609 Knockdown Suppresses Cell Growth via Modulating miR-188/ELF2 Axis in Nasopharyngeal Carcinoma</p>

2020

OTT

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Background: Circular RNAs (circRNAs) and microRNAs (miRNAs) have been reported to act as the important regulators in nasopharyngeal carcinoma (NPC). CircRNA ZNF609 (circ-ANF609) and miR-188 have been, respectively, reported to play a pro-cancer and anti-cancer role in NPC. The purpose of this study is to reveal the functional relation of circ-ZNF609 and miR-188 in NPC development. Methods: The transcription level and protein level of genes were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assay, respectively. Cell proliferation was analyzed using 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Furthermore, flow cytometry analysis was used to assess cell cycle transition and cell apoptosis rate. Besides, the interaction between miR-188 and circ-ZNF609 or E74-like factor 2 (ELF2) was predicted by starbase or microT-CDS, and then confirmed by the dual luciferase reporter assay and RIP assay. Results: Circ-ZNF609 and ELF2 levels were increased and miR-188 level was decreased in NPC. Circ-ZNF609 knockdown significantly inhibited cell proliferation and cell cycle transition, as well as accelerated apoptosis in NPC cells. Interestingly, circ-ZNF609 directly bound to miR-188. Circ-ZNF609 regulated NPC cell growth through modulating miR-188 expression. In addition, miR-188 suppressed NPC cell growth via directly targeting ELF2. Finally, we confirmed that circ-ZNF609 mediated miR-188 level to modulate ELF2 expression. Conclusion: Our findings demonstrated that circ-ZNF609 depletion-repressed proliferation and cell cycle transition, and induced apoptosis of NPC cells via modulation of miR-188/ ELF2 axis, providing potential targets for the therapy of NPC.

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“…Therefore, it is of great significance to find novel and invaluable prognostic biomarkers for glioma patients. Nowadays, increasing studies have proved that a series of miRNAs are involved in progression of multiple styles of tumors [7][8][9][10][11][12][13]. For instance, miR-662 [6], miR-532-5p [14], miR-199a [15], miR-940 [24], miR-200b [17], miR-34a [18], miR-130b [19], and miR-148a [20] all play an essential role in gliomas.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-136-3p inhibits glioma tumorigenesis in vitro and in vivo by targeting KLF7

Xu¹

2020

World J Surg Onc

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Background: Malignant brain tumors have been a serious threat to human health worldwide. This study aims to investigate the role of miR-136-3p in glioma development. Methods: Hematoxylin-eosin staining (H&E) staining was used to determine the pathologic alterations of glioma tissues. Quantitative real-time PCR (qRT-PCR) analysis and GEO2R analysis was performed to examine the expression of miRNAs and genes. Western blot was applied to detect the protein expression. Cell counting kit-8 (CCK-8) and colony formation were used to analyze the glioma cell growth. Trans-well assay was used to determine the cell migration. Annexin V-FITC/PI staining was conducted to determine the cell apoptosis of transfected glioma cells. The dual-luciferase reporter assay was carried out to confirm the binding sites of miR-136-3p on 3′ untranslated regions (3′ UTR) of Kruppel-like factor 7 (KLF7). Tumor-bearing experiment in nude mice was performed to comprehensively investigate the role of miR-136-3p/KLF7 axis in gliomas. Results: Firstly, the results showed that miR-136-3p was decreased in glioma tissues compared with adjacent tissues. Overexpression of miR-136-3p significantly inhibited cell growth of LN-229 and U251 by decreasing expression of Cyclin A1 and PCNA (proliferating cell nuclear antigen), and it suppressed glioma cell migration by downregulating N-cadherin and elevating E-cadherin levels, and it also promotes glioma cell apoptosis by promoting Bcl2-associated X (Bax) expression but suppressing Bcl-2 expression. Furthermore, we observed that KLF7 was a direct target of miR-136-3p, and KLF7 was negatively regulated by miR-136-3p in glioma cells. Finally, overexpression of KLF7 partly blocked miR-136-3p-induced inhibition of tumor growth in vitro and in vivo. Conclusions: Targeting miR-136-3p/KLF7 axis might be a novel manner to counter against gliomas.

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miRNA-Dependent Activation of mRNA Translation

Cited by 58 publications

References 0 publications

Hemorrhage enhances cytokine, complement component 3, and caspase-3, and regulates microRNAs associated with intestinal damage after whole-body gamma-irradiation in combined injury

Hemorrhage enhances cytokine, complement component 3, and caspase-3, and regulates microRNAs associated with intestinal damage after whole-body gamma-irradiation in combined injury

<p>CircRNA ZNF609 Knockdown Suppresses Cell Growth via Modulating miR-188/ELF2 Axis in Nasopharyngeal Carcinoma</p>

MicroRNA-136-3p inhibits glioma tumorigenesis in vitro and in vivo by targeting KLF7

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