Project description:Long non-coding RNA NR2F1 antisense RNA1 (lncRNA NR2F1-AS1) was identified as the main candidate associated to late recurrence in ER-positive breast cancer clinical samples. Gain-of-function of NR2F1-AS1 induced the expression of dormancy-inducers BMP4 and DEC2, and upregulated pluripotency markers NANOG and OCT4. Representative pathways entailed to metastatic events such as HER2/Neu, hypoxia, EMT and inflammatory-response were also found enriched.
Project description:Long non-coding RNA NR2F1 antisense RNA1 (lncRNA NR2F1-AS1) was identified as the main candidate associated to late recurrence in ER-positive breast cancer clinical samples. Gain-of-function of NR2F1-AS1 induced the expression of dormancy-inducers BMP4 and DEC2, and upregulated pluripotency markers NANOG and OCT4. Representative pathways entailed to metastatic events such as HER2/Neu, hypoxia, EMT and inflammatory-response were also found enriched.
Project description:Our data showed that NR2F1-AS1 functions oncogenic roles in gastric cancer (GC), but the underlying molecular mechanism remains largely unknown to date. To explore the function of lncRNA NR2F1-AS1 in gastric cancer, loss-of-function and RNA sequencing studies were performed in SGC7901 cell line. The results showed that depletion of NR2F1-AS1 significantly decreased the expression of VAMP7. Interestingly, VAMP7 was also a target gene of miR-29a-3p. Our data showed that NR2F1-AS1 promotes GC progression through regulating miR-29a/VAMP7 axis.
Project description:We show that the epithelial-like and mesenchymal-like subpopulations of breast cancer stem-like cells (BCSCs) demonstrate different levels dormancy and tumorigenicity in lungs. The long non-coding RNA (lncRNA) molecule NR2F1-AS1 (NAS1) is up-regulated in the dormant BCSC subpopulation, and functionally promotes tumor dissemination but reduces proliferation in lungs. Mechanically, NAS1 promotes internal ribosome entry site (IRES)-mediated NR2F1 translation, leading to inhibition of ΔNp63 transcription by NR2F1. Further, ΔNp63 downregulation results in epithelial-mesenchymal transition, reduced tumorigenicity and enhanced dormancy of cancer cells in lungs.
Project description:NFYC-AS1 is an overlapping antisense RNA transcribed head-to-head to NFYC sense gene, encoding for the subunit C of NF-Y transcription factor, which is known as master regulator of cell cycle and proliferation in normal and tumor cells. Here we performed NFYC-AS1 silencing in lung squamous carcinoma H520 cells by Gapmer antisense oligonucleotides and CRISPR/Cas9 TSS deletion. Afterwards, we performed differentially expressed analysis and gene set enrichement analysis to investigate on NFYC-AS1 function and mechanism of action.
Project description:Characterisation IER3-AS1 interacting proteins using chromatin oligo-affinity precipitation (ChOP) followed by mass spectrometry. The HeLa cell lysates was incubated with biotinylated antisense oligonucleotides (ASO), targeting an experimental target antisense long noncoding RNA IER3-AS1 or a control RNA LacZ. LacZ and IER3-AS1 interacting proteomes were pulldown using Streptavidin beads. The eluted protein samples from both LacZ control ASOs and IER3-AS1 ASOs subjected to mass-spectrometry analyses to identify IER3-AS1 interacting proteins.
Project description:LncRNA Hypoxia-inducible factor 1α-antisense 1 (HIF1α-AS1) is located on the antisense strand of the important Hypoxia-inducible factor 1α (HIF1α) gene, but being transcribed in antisense direction along the HIF1α promoter. Here we used the 3’end biotinylated HIF1a-AS1 RNA and a control RNA for RNA Pulldown and searched for interacting proteins in nuclear extracts of human umbilical vein endothelial cells (HUVEC).
Project description:Monocytes are key players in innate immunity, with their ability to regulate inflammatory responses and combat invading pathogens. There is a growing body of evidence indicating that long non-coding RNA (lncRNA) participate in various cellular biological processes, including the innate immune response. The immunoregulatory properties of numerous lncRNAs discovered in monocytes remain largely unexplored. In this study, we used RNA sequencing data of circulatory blood monocytes obtained from sepsis patients to identify the elevated antisense lncRNA JHMD1D-AS1, relative to healthy participants. We subsequently demonstrated that in both circulatory blood monocytes and monocyte-derived macrophages exposed to TLR-agonists, JHMD1D-AS1 expression was induced in a temporal specific manner. Using small interfering RNA (siRNA) electroporation to render monocytes deficient of JHDM1D-AS1 and over-expression experiments, we revealed a role for lncRNA JHDM1D-AS1 in cell development, as well as in restraining pro-inflammatory gene expression. Altogether, these findings identify antisense lncRNA JHDM1D-AS1 as a potential repressor of the inflammatory response in human primary monocytes and macrophages.