Non-coding RNAs in Transcriptional Regulation

Chen, Yung-Chia Ariel; Aravin, Alexei A.

doi:10.1007/s40610-015-0002-6

Cited by 36 publications

(17 citation statements)

References 93 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Long non-coding RNAs, also known as lncRNAs, have recently received wide attention due to their rising functions in development and diseases 8 , 9 . Such RNA transcripts are characterized by more than 200 nucleotides that have no capacity of encoding proteins 10 . Increasing evidence has shown that lncRNAs are involved in several levels, including transcription and post-transcription 11 - 13 .…”

Section: Introductionmentioning

confidence: 99%

LncRNA AFAP1-AS Functions as a Competing Endogenous RNA to Regulate RAP1B Expression by sponging miR-181a in the HSCR

Chen¹,

Peng²,

Zhu³

et al. 2017

Int. J. Med. Sci.

View full text Add to dashboard Cite

Background: Long noncoding RNAs (lncRNAs) have recently emerged as important regulators in a broad spectrum of cellular processes including development and disease. Despite the known engagement of the AFAP1-AS in several human diseases, its biological function in Hirschsprung disease (HSCR) remains elusive.Methods: We used qRT-PCR to detect the relative expression of AFAP1-AS in 64 HSCR bowel tissues and matched normal intestinal tissues. The effects of AFAP1-AS on cell proliferation, migration, cell cycle, apoptosis and cytoskeletal organization were evaluated using CCK-8, transwell assay, flow cytometer analysis and immunofluorescence, in 293T and SH-SY5Y cell lines, respectively. Moreover, the competing endogenous RNA (ceRNA) activity of AFAP1-AS on miR-181a was investigated via luciferase reporter assay and immunoblot analysis.Results: Aberrant inhibition of AFAP1-AS was observed in HSCR tissues. Knockdown of AFAP1-AS in 293T and SH-SY5Y cells suppressed cell proliferation, migration, and induced the loss of cell stress filament integrity, possibly due to AFAP1-AS sequestering miR-181a in HSCR cells. Furthermore, AFAP1-AS could down-regulate RAP1B via its competing endogenous RNA (ceRNA) activity on miR-181a.Conclusions: These findings suggest that aberrant expression of lncRNA AFAP1-AS, a ceRNA of miR-181a, may involve in the onset and progression of HSCR by augmenting the miR-181a target gene, RAP1B.

show abstract

Section: Introductionmentioning

confidence: 99%

LncRNA AFAP1-AS Functions as a Competing Endogenous RNA to Regulate RAP1B Expression by sponging miR-181a in the HSCR

Chen¹,

Peng²,

Zhu³

et al. 2017

Int. J. Med. Sci.

View full text Add to dashboard Cite

show abstract

“…During the post-genome period, lncRNAs have become a focus of study in the regulation of histone acetylation, gene methylation, post-transcription translation, and other biological processes [ 23 - 25 ]. Recently, many more lncRNAs have been confirmed to play critical roles in regulating the physiological behavior of malignant cancers, including breast, pancreatic, gastric, lung, and others.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, lncRNAs have attracted much attention in various areas of study to elucidate the complex mechanisms of multiple cellular processes, especially in cancer [ 20 - 22 ]. The functions of lncRNAs mainly include regulation of gene methylation, transcriptional activation, conjugation with mRNAs and miRNAs to affect translation progression and other processes [ 23 - 25 ]. Normally, the relationships between lncRNAs and their neighboring coding genes include sense overlapping, antisense, intronic, divergent, and intergenic interactions [ 26 , 27 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer

et al. 2016

Oncotarget

View full text Add to dashboard Cite

Triple negative breast cancer (TNBC) is an aggressive type of breast cancer with high heterogeneity. To date, there is no efficient therapy for TNBC patients and the prognosis is poor. It is urgent to find new biomarkers for the diagnosis of TNBC or efficient therapy targets. As an area of focus in the post-genome period, long non-coding RNAs (lncRNAs) have been found to play critical roles in many cancers, including TNBC. However, there is little information on differentially expressed lncRNAs between TNBC and non-TNBC. We detected the expression levels of lncRNAs in TNBC and non-TNBC tissues separately. Then we analyzed the lncRNA expression signature of TNBC relative to non-TNBC, and found dysregulated lncRNAs participated in important biological processes though Gene Ontology and Pathway analysis. Finally, we validated these lncRNA expression levels in breast cancer tissues and cells, and then confirmed that 4 lncRNAs (RP11-434D9.1, LINC00052, BC016831, and IGKV) were correlated with TNBC occurrence through receiver operating characteristic curve analysis. This study offers helpful information to understand the initiation and development mechanisms of TNBC comprehensively and suggests potential biomarkers for diagnosis or therapy targets for clinical treatment.

show abstract

“…LncRNAs are a form of RNA whose length is more than 200 nucleotides. They themselves do not encode proteins but participate in the regulation of gene expression and various biological processes [ 5 ]. LncRNAs can activate or inhibit the expression of target genes by directly binding to the target genes, or be involved in histone modification or recruitment of transcription factors.…”

Section: Introductionmentioning

confidence: 99%

A transcribed ultraconserved noncoding RNA, Uc.173, is a key molecule for the inhibition of lead-induced neuronal apoptosis

et al. 2015

View full text Add to dashboard Cite

As a common toxic metal, lead has significant neurotoxicity to brain development. Long non-coding RNAs (lncRNAs) function in multiple biological processes. However, whether lncRNAs are involved in lead-induced neurotoxicity remains unclear. Uc.173 is a lncRNA from a transcribed ultra-conservative region (T-UCR) of human, mouse and rat genomes. We established a lead-induced nerve injury mouse model. It showed the levels of Uc.173 decreased significantly in hippocampus tissue and serum of the model. We further tested the expression of Uc.173 in serum of lead-exposed children, which also showed a tendency to decrease. To explore the effects of Uc.173 on lead-induced nerve injury, we overexpressed Uc.173 in an N2a mouse nerve cell line and found Uc.173 had an inhibitory effect on lead-induced apoptosis of N2a. To investigate the molecular mechanisms of Uc.173 in apoptosis associated with lead-induced nerve injury, we predicted the target microRNAs of Uc.173 by using miRanda, TargetScan and RegRNA. After performing quantitative real-time PCR and bioinformatics analysis, we showed Uc.173 might inter-regulate with miR-291a-3p in lead-induced apoptosis and regulate apoptosis-associated genes. Our study suggests Uc.173 significantly inhibits the apoptosis of nerve cells, which may be mediated by inter-regulation with miRNAs in lead-induced nerve injury.

show abstract

Non-coding RNAs in Transcriptional Regulation

Cited by 36 publications

References 93 publications

LncRNA AFAP1-AS Functions as a Competing Endogenous RNA to Regulate RAP1B Expression by sponging miR-181a in the HSCR

LncRNA AFAP1-AS Functions as a Competing Endogenous RNA to Regulate RAP1B Expression by sponging miR-181a in the HSCR

LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer

A transcribed ultraconserved noncoding RNA, Uc.173, is a key molecule for the inhibition of lead-induced neuronal apoptosis

Contact Info

Product

Resources

About