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Genome-Wide CRISPR-Cas9 Screen Identifies MicroRNAs That Regulate Myeloid Leukemia Cell Growth. | LitMetric

AI Article Synopsis

  • Mammalian microRNA expression is often disrupted in cancer, but their specific roles in tumors are not well understood.
  • Researchers used CRISPR-Cas9 technology to conduct a comprehensive screen of microRNAs and protein-coding genes in a myeloid leukemia cell line, finding that certain microRNAs can either inhibit or promote cell growth.
  • The study highlighted miR-155 as a key microRNA that enhances cell survival and identified its relationship with tumor suppressor p53, demonstrating a valuable method for exploring microRNA functions in cancer.

Article Abstract

Mammalian microRNA expression is dysregulated in human cancer. However, the functional relevance of many microRNAs in the context of tumor biology remains unclear. Using CRISPR-Cas9 technology, we performed a global loss-of-function screen to simultaneously test the functions of individual microRNAs and protein-coding genes during the growth of a myeloid leukemia cell line. This approach identified evolutionarily conserved human microRNAs that suppress or promote cell growth, revealing that microRNAs are extensively integrated into the molecular networks that control tumor cell physiology. miR-155 was identified as a top microRNA candidate promoting cellular fitness, which we confirmed with two distinct miR-155-targeting CRISPR-Cas9 lentiviral constructs. Further, we performed anti-correlation functional profiling to predict relevant microRNA-tumor suppressor gene or microRNA-oncogene interactions in these cells. This analysis identified miR-150 targeting of p53, a connection that was experimentally validated. Taken together, our study describes a powerful genetic approach by which the function of individual microRNAs can be assessed on a global level, and its use will rapidly advance our understanding of how microRNAs contribute to human disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4833428PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0153689PLOS

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