| Literature DB >> 29677511 |
Assaf C Bester1, Jonathan D Lee1, Alejandro Chavez2, Yu-Ru Lee1, Daphna Nachmani1, Suhani Vora3, Joshua Victor1, Martin Sauvageau4, Emanuele Monteleone5, John L Rinn6, Paolo Provero7, George M Church3, John G Clohessy8, Pier Paolo Pandolfi9.
Abstract
Resistance to chemotherapy plays a significant role in cancer mortality. To identify genetic units affecting sensitivity to cytarabine, the mainstay of treatment for acute myeloid leukemia (AML), we developed a comprehensive and integrated genome-wide platform based on a dual protein-coding and non-coding integrated CRISPRa screening (DICaS). Putative resistance genes were initially identified using pharmacogenetic data from 760 human pan-cancer cell lines. Subsequently, genome scale functional characterization of both coding and long non-coding RNA (lncRNA) genes by CRISPR activation was performed. For lncRNA functional assessment, we developed a CRISPR activation of lncRNA (CaLR) strategy, targeting 14,701 lncRNA genes. Computational and functional analysis identified novel cell-cycle, survival/apoptosis, and cancer signaling genes. Furthermore, transcriptional activation of the GAS6-AS2 lncRNA, identified in our analysis, leads to hyperactivation of the GAS6/TAM pathway, a resistance mechanism in multiple cancers including AML. Thus, DICaS represents a novel and powerful approach to identify integrated coding and non-coding pathways of therapeutic relevance.Entities:
Keywords: AML; AXL/GAS6; CRISPR; CRISPRa; TEM; cancer; cytarabine; drug-resistance; leukemia; lncRNA
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Year: 2018 PMID: 29677511 PMCID: PMC6061940 DOI: 10.1016/j.cell.2018.03.052
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582