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Role of ADAR1 on transcriptional output in cancer cells

ABSTRACT: Role of ADAR1 on transcriptional output in cancer cells

PROVIDER: PRJNA1152573 | ENA |

REPOSITORIES: ENA

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Role of ADAR1 on transcriptional output in cancer cells

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ADAR1 regulates growth & invasion in triple-negative breast cancer

Project description:ADAR1 catalyzes Adenosine-to-Inosine (A-to-I) editing of double-stranded RNA and regulates global expression output through its interactions with RNA and other proteins. ADARs play important roles in development and disease, and previous work has shown that ADAR1 is oncogenic in a growing list of cancer types. Here we show that ADAR1 is important for growth and invasion in triple negative breast cancer cells, as ADAR1 loss yields reduced growth, migration & invasion, and mammosphere formation. Global RNA-seq analyses demonstrate that ADAR1 regulates both coding and non-coding targets via expression level and/or A-to-I editing. We demonstrated that a recoding edit in FLNB (chr3:58156064) inhibits the tumor suppressive activities of the protein to promote growth & invasion. We show that several tumor suppressor microRNAs are also downregulated by ADAR1 to promote cell cycle progression and invasion. This work describes several novel mechanisms of ADAR1-mediated oncogenesis in triple negative breast cancer, providing support to strategies for targeting ADAR1 in this aggressive cancer type with few treatment options.

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Role of ADAR1 in human macrophages

Project description:This study aims to delineate the role of ADAR1 in human cells beyond its canonical function as an interferon-stimulated gene (ISG). Human monocyte-derived macrophages were subjected to RNA interference targeting either pan-ADAR1 (both isoforms) or the p150 isoform specifically. Quantitative proteomic analyses were performed using state-of-the-art isobaric tandem mass tag (TMT) labeling coupled with liquid chromatography–tandem mass spectrometry (LC-MS/MS). Strikingly, silencing of ADAR1 significantly impacted prototypical macrophage functions, including endocytosis, cholesterol metabolism, and lysosomal processing, without concurrent induction of pro-inflammatory or ISG responses. Pan-ADAR1 silencing resulted in upregulation of proteins involved in lysosomal function and cholesterol processing, whereas selective depletion of ADAR1-p150 led to downregulation of pathways associated with phagocytosis and endocytosis. Moreover, loss of pan-ADAR1 caused a marked downregulation of cell-cycle and p53 signaling pathways, suggesting a potential role for the ADAR1-p110 isoform in regulating cell proliferation. Collectively, these data define previously unappreciated proteomic alterations driven by ADAR1 that influence fundamental macrophage functions beyond its established ISG role.

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