Cancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA; Ludwig Center at Harvard, Harvard Medical School, Boston, MA, USA.
Wyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA; Department of Pathology and Cell Biology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA; Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
Cell. 2018 Apr 19;173(3):649-664.e20. doi: 10.1016/j.cell.2018.03.052.
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.
化疗耐药在癌症死亡率中起着重要作用。为了确定影响阿糖胞苷敏感性的遗传单元,阿糖胞苷是治疗急性髓细胞白血病(AML)的主要药物,我们开发了一种基于双蛋白编码和非编码整合 CRISPRa 筛选(DICaS)的全面综合基因组平台。最初使用来自 760 个人类泛癌细胞系的药物遗传学数据来鉴定潜在的耐药基因。随后,通过 CRISPR 激活对编码和长非编码 RNA(lncRNA)基因进行了全基因组功能特征分析。为了评估 lncRNA 的功能,我们开发了一种靶向 14701 个 lncRNA 基因的 CRISPR 激活 lncRNA(CaLR)策略。计算和功能分析鉴定了新的细胞周期、存活/凋亡和癌症信号基因。此外,我们的分析中鉴定的 GAS6-AS2 lncRNA 的转录激活导致 GAS6/TAM 途径的过度激活,这是包括 AML 在内的多种癌症的一种耐药机制。因此,DICaS 代表了一种识别治疗相关的整合编码和非编码途径的新的、强大的方法。