Short-lived long non-coding RNAs as surrogate indicators for chemical exposure and LINC00152 and MALAT1 modulate their neighboring genes.
Hidenori TaniSayaka OkudaKaoru NakamuraMotohide AokiTomonari UmemuraPublished in: PloS one (2017)
Whole transcriptome analyses have revealed a large number of novel long non-coding RNAs (lncRNAs). Although accumulating evidence demonstrates that lncRNAs play important roles in regulating gene expression, the detailed mechanisms of action of most lncRNAs remain unclear. We previously reported that a novel class of lncRNAs with a short half-life (t1/2 < 4 h) in HeLa cells, termed short-lived non-coding transcripts (SLiTs), are closely associated with physiological and pathological functions. In this study, we focused on 26 SLiTs and nuclear-enriched abundant lncRNA, MALAT1(t1/2 of 7.6 h in HeLa cells) in neural stem cells (NSCs) derived from human induced pluripotent stem cells, and identified four SLiTs (TUG1, GAS5, FAM222-AS1, and SNHG15) that were affected by the following typical chemical stresses (oxidative stress, heavy metal stress and protein synthesis stress). We also found the expression levels of LINC00152 (t1/2 of 2.1 h in NSCs), MALAT1 (t1/2 of 1.8 h in NSCs), and their neighboring genes were elevated proportionally to the chemical doses. Moreover, we confirmed that the overexpression of LINC00152 or MALAT1 upregulated the expressions of their neighboring genes even in the absence of chemical stress. These results reveal that LINC00152 and MALAT1 modulate their neighboring genes, and thus provide a deeper understanding of the functions of lncRNAs.
Keyphrases
- long non coding rna
- poor prognosis
- genome wide identification
- genome wide analysis
- genome wide
- cell cycle arrest
- induced apoptosis
- induced pluripotent stem cells
- gene expression
- transcription factor
- oxidative stress
- dna methylation
- heavy metals
- network analysis
- single cell
- bioinformatics analysis
- neural stem cells
- cell death
- endoplasmic reticulum stress
- cell proliferation
- pi k akt
- endothelial cells
- signaling pathway
- stress induced
- rna seq
- risk assessment
- dna damage
- ischemia reperfusion injury
- room temperature
- diabetic rats
- binding protein