Faculty Opinions recommendation of GW182 proteins cause PABP dissociation from silenced miRNA targets in the absence of deadenylation.

Author(s):  
Martin Jinek
Keyword(s):  
2021 ◽  
Vol 160 (1) ◽  
pp. 97-111
Author(s):  
Ting Li ◽  
Nianjiao Tao ◽  
Yuanmi Lin ◽  
Min Chen ◽  
Dongli Jiao ◽  
...  

2010 ◽  
Vol 12 (2) ◽  
pp. 115-121 ◽  
Author(s):  
X. Dai ◽  
Z. Zhuang ◽  
P. X. Zhao

Methods ◽  
2012 ◽  
Vol 58 (2) ◽  
pp. 94-105 ◽  
Author(s):  
Markus Hafner ◽  
Steve Lianoglou ◽  
Thomas Tuschl ◽  
Doron Betel
Keyword(s):  

Author(s):  
Gongping Sun ◽  
He Duan ◽  
Jin Meng ◽  
Dewei Zhang

Background: Short-chain fatty acids exert anti-cancer effects on tumor cells. Objective: We aimed to reveal the signaling network altered by butyrate in Gastric Cancer (GC) using small RNA sequencing (sRNA-seq). Methods: The effects of butyrate on the biological behavior of NCI-N87 and KATO III cells in vitro were assessed by functional assays and half-maximal inhibitory concentrations (IC50) of butyrate in KATO III cells were calculated. sRNA-seq was performed on KATO III cells. Differentially expressed miRNAs (DE-miRNAs) were identified between butyrate treatment and control groups using DESeq2, and miRNA targets were predicted. A protein-protein interaction (PPI) network of DE-miRNA targets was created using Metascape. Key MCODE complexes were identified using the MCODE algorithm and cluster Profiler. The relationship between DE-miRNA and GC overall survival (OS) was evaluated using Kaplan-Meier curves. Results: Butyrate dose-dependently inhibited NCI-N87 and KATO III cell viability. KATO III cells were more sensitive to butyrate than NCI-N87 cells. Butyrate promoted apoptosis and inhibited KATO III cell migration. Total 324 DE-miRNAs were identified in KATO III cells, and 459 mRNAs were predicted as targets of 83 DE-miRNAs. Two key protein complexes were identified in a PPI network of the 459 targets. A key signaling network responding to butyrate were generated using targets in these key complexes and their miRNA regulators. The DE-miRNAs in the key signaling network were related to the OS of GC. Conclusion: Butyrate altered the biological behavior of GC cells, which may be achieved by regulating miRNAs and related oncogenic pathways.


Author(s):  
Matthew J. Coussens ◽  
Kevin Forbes ◽  
Carol Kreader ◽  
Jack Sago ◽  
Carrie Cupp ◽  
...  
Keyword(s):  

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Xin Zhao ◽  
Dongyang Tang ◽  
Xiaofei Chen ◽  
Shaoqing Chen ◽  
Cheng Wang

Introduction. Baicalein has been shown to have antitumor activities in several cancer types. However, its acting mechanisms remain to be further investigated. This work is aimed at exploring the functional long noncoding RNA (lncRNA)/microRNA (miRNA)/messenger RNA (mRNA) triplets in response to baicalein in hepatocellular carcinoma (HCC) cell to understand the mechanisms of baicalein in HCC. Methods. Differentially expressed lncRNAs (DELs) and miRNAs (DEMs) in HCC cell treated with baicalein were first screened using GSE95504 and GSE85511, respectively. miRNA targets for DELs were predicted and intersected with DEMs, after which the miRNA expression was validated using ENCORI and its prognostic value was assessed using Kaplan-Meier plotter. Potential miRNA targets were predicted by 3 prediction tools, after which expression level was validated at UALCAN and Human Protein Atlas. Kaplan-Meier plotter was used to evaluate the effects of these genes on overall survival and recurrence-free survival of HCC patients. Enrichment analyses for these genes were performed at DAVID. Results. Here, we identified 14 overlapping DELs and 26 overlapping DEMs in the baicalein treatment group than those in the DMSO treatment group. Subsequently, by analyzing expression and clinical significance of miRNAs, hsa-miR-4443 was found as a highly potential miRNA target. Then, targets of hsa-miR-4443 were predicted and analyzed, and we found AKT1 was the most potential target for hsa-miR-4443. Hence, the lncRNAs-hsa-miR-4443-AKT1 axis that can respond to baicalein was established. Conclusion. Collectively, we elucidated a role of lncRNAs-hsa-miR-4443-AKT1 pathway in response to baicalein treatment in HCC, which could help us understand the roles of baicalein in inhibiting cancer progression and may provide novel insights into the mechanisms behind HCC progression.


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