Project description:By using shRNAs the lnc-klhdc7b was silenced in the cell line HCC1187, the shRNA-1 carried a ~75% silencing compared to the negative control (NC). We evaluated the role of LncKLHDC7B on oncogenic phenotypes in the IM breast cancer HCC1187 cell line model. The knockdown of LncKLHDC7B was achieved with ~75% of silencing efficiency. A complete genomic analysis of the transcriptomic state after silencing of LncKLHDC7B revealed an impact on the global expression of transcripts
Project description:Kelch domain-containing 7B (KLHDC7B) was revealed hypermethylated at promoter but upregulated in breast cancer. And we identified a long non-coding RNA, ST8SIA6-AS1 (STAR1), of which expression was highly associated with KLHDC7B in breast cancer (r = 0.5887).
Project description:Kelch domain-containing 7B (KLHDC7B) was revealed hypermethylated at promoter but upregulated in breast cancer. And we identified a long non-coding RNA, ST8SIA6-AS1 (STAR1), of which expression was highly associated with KLHDC7B in breast cancer (r = 0.5887).
Project description:To gain more insights into the functional significance of lnc-HLX-2-7 in human medulloblastoma, genomic mapping of lnc-HLX-2-7 occupancy were analyzied by ChIRP DNA sequencing.
Project description:Kelch domain-containing 7B (KLHDC7B) was revealed hypermethylated at promoter but upregulated in breast cancer. And we identified a long non-coding RNA, ST8SIA6-AS1 (STAR1), of which expression was highly associated with KLHDC7B in breast cancer (r = 0.5887).
Project description:Endogenous retroviruses (ERVs) are transposable elements that cause host genome instability and usually play deleterious roles such as tumorigenesis. Recent advances also suggest that this 'enemy within' may encode viral mimic to induce antiviral immune responses through viral sensors. Here, through whole genome RNA-seq we discovered a full-length ERV-derived long non-coding RNA (lncRNA), designated lnc-EPAV (ERV-derived lncRNA positively regulates antiviral responses), as a positive regulator of NF-κB signaling. Lnc-EPAV expression was rapidly up-regulated by viral RNA mimic or RNA viruses to facilitate the expression of RELA, an NF-κB subunit that plays a critical role in antiviral responses. In turn, RELA promoted the transcription of lnc-EPAV to form a positive feedback loop. Transcriptome analysis of lnc-EPAV-silenced macrophages, combined with gain- and loss-of-function experiments, showed that lnc-EPAV was critical for induction of type I interferon (IFN) and inflammatory cytokine expression by RNA viruses. Consistently, lnc-EPAV-deficient mice exhibited reduced expression of type I IFNs, and consequently increased viral loads and mortality following lethal RNA virus infection. Mechanistically, lnc-EPAV promoted expression of RELA by competitively binding to and displacing SFPQ, a transcriptional repressor of RELA. The binding between ERV-derived RNAs and SFPQ also existed in human cells. Altogether, our work demonstrates an alternative mechanism by which ERVs regulate antiviral immune responses.
Project description:Overwhelming evidence indicates that long non-coding RNAs have essential roles in tumorigenesis. Nevertheless, their expression and role in pediatric B-cell precursor acute lymphoblastic leukemia has not been extensively explored. Here, we conducted a comprehensive analysis of the long non-coding RNA transcriptome in ETV6/RUNX1 positive BCP-ALL, one of the most frequent subtypes of pediatric leukemia. An ETV6/RUNX1 expression signature was established, consisting of 596 lncRNAs (434 up and 162 down) using expression analysis of a series of primary patient samples. Subsequently, RNA sequencing from BCP-ALL cell lines and shRNA-mediated silencing of ETV6/RUNX1, illustrated that lnc-NKX2-3-1, lnc-TIMM21-5, lnc-ASTN1-1 and lnc-RTN4R-1 are bona fide ETV6/RUNX1 targets and could serve as novel biomarkers of this prevalent subtype of human leukemia.