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Series GSE147487 Query DataSets for GSE147487
Status Public on Sep 17, 2020
Title RNA editing in cancer impacts mRNA abundance in immune response pathways
Organism Homo sapiens
Experiment type Expression profiling by high throughput sequencing
Summary RNA editing generates modifications to RNA sequences, thereby increasing protein diversity and shaping various layers of gene regulation. Recent studies have revealed global shifts in editing levels across many cancer types, as well as a few specific mechanisms implicating individual sites in tumorigenesis or metastasis. However, most tumor-associated sites, predominantly in noncoding regions, have unknown functional relevance. Here, we carry out integrative analysis of RNA editing profiles between epithelial (E) and mesenchymal (M) tumors, since epithelial-mesenchymal transition (EMT) is a key paradigm for metastasis. We identify distinct editing patterns between E and M tumors in seven cancer types using TCGA data, an observation further supported by single-cell RNA-seq data and ADAR perturbation experiments in cell culture. Through computational analyses and experimental validations, we show that differential editing sites between E and M phenotypes function by regulating mRNA abundance of their respective genes. Our analysis of >120 RNA-binding proteins revealed ILF3 as a potential regulator of this process, supported by experimental validations. Consistent with the known roles of ILF3 in immune response, E-M differential editing sites are enriched in genes involved in immune and viral processes. The strongest target of editing-dependent ILF3 regulation is the transcript encoding PKR, a crucial player in immune and viral response. Our study reports widespread differences in RNA editing between epithelial and mesenchymal tumors and a novel mechanism of editing-dependent regulation of mRNA abundance. It reveals the broad impact of RNA editing in cancer and its relevance to cancer-related immune pathways.
Overall design eCLIP-seq in A549 cells.
RNA-seq in A549 cells upon knockdown of ADARs.
Contributor(s) Chan T, Fu T, Bahn JH, Jun H, Lee J, Quinones-Valdez G, Cheng C, Xiao X
Citation(s) 33106178
Submission date Mar 24, 2020
Last update date Nov 02, 2020
Contact name Xinshu Xiao
Organization name University of California, Los Angeles
Street address 610 Charles E. Young Drive S
City Los Angeles
State/province CA
ZIP/Postal code 90095-1570
Country USA
Platforms (2)
GPL20301 Illumina HiSeq 4000 (Homo sapiens)
GPL21290 Illumina HiSeq 3000 (Homo sapiens)
Samples (15)
GSM4431931 ILF3_IPA
GSM4431932 ILF3_IPB
GSM4431933 SMInput
BioProject PRJNA614963
SRA SRP253895

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Supplementary file Size Download File type/resource
GSE147487_ILF3_A549.both_reps_and_alu.gene_annotated.alu_annotated.bed.gz 1.4 Mb (ftp)(http) BED
GSE147487_siADARs_A549.TPM.txt.gz 2.2 Mb (ftp)(http) TXT
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Raw data are available in SRA
Processed data are available on Series record

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