Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA312905 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3183631.fastq.gz | Fastqsanger.gz | |||
| SRR3183632.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: To identify all of the APA targets of CFIm25 on a global scale and develop an algorithm that can idenitify APA events from standard RNA-seq data Methods: RNA from HeLa cells treated with control siRNA and CFIm25 siRNA were subject to RNA-Seq. Using a custom-designed algorithm to mine RNA-seq data for novel APA events regulated by CFIm25. Results: We identified over 1,400 genes with shortened 3’UTRs after CFIm25 knockdown. Importantly, we show that as a consequence of APA, many of these mRNAs have greatly enhanced protein expression due to the loss of destabilizing features within the 3’UTR. Conclusions: Our study underscored the critical function of the CFIm complex members in governing APA and establish a previously unknown link between APA and metabolic pathways important for tumor progression. Hela cell line mRNA profiles of control treated and CFIm25 Knockdown were generated by RNA-Seq using Illumina GAIIx.
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Project description:Purpose: When CFIm25 knockdown induces global APA events, we aim to investigate ceRNA landscape change based on microRNA expression change. Methods: microRNA from HeLa cells treated with control siRNA and CFIm25 siRNA were subject to RNA-Seq. Results: Consistent with our observations in TCGA breast cancer, we found a surprisingly high enrichment of 3ʹUTR shortening genes' ceRNA partners to tumor suppressors and their down-regulation. Conclusion: Our work indicated that the shortened 3ʹ-UTRs might direct the released miRNAs to repress their ceRNA partners in trans, which are enriched in ceRNET hubs and tumor suppressors, thereby effectively disrupting normal ceRNET and contributing to tumorigenesis.
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