SGOL1-AS1 enhances cell survival in Acute Myeloid Leukemia by maintaining pro-inflammatory signaling

Ewan Selkirk, Rahima Patel, Anna Hoyle, Michael Lie-A-Ling, Duncan Smith, Joe Swift, Georges Lacaud

Research output: Contribution to journalArticlepeer-review


Epigenetic dysregulation is a key feature of most acute myeloid leukemia (AML). Recently, it has become clear that long noncoding RNAs (lncRNAs) can play a key role in epigenetic regulation, and consequently also dysregulation. Currently, our understanding of the requirements and roles of lncRNAs in AML is still limited. Here, using CRISPRi screening, we identified the lncRNA SGOL1-AS1 as an essential regulator of survival in THP-1 AML cells. We demonstrated that SGOL1-AS1 interacts with chromatin-modifying proteins involved in gene repression and that SGOL1-AS1 knockdown is associated with increased heterochromatin formation. We also observed that loss of SGOLl-AS1 results in increased apoptosis and the downregulation of pro-inflammatory genes. In AML patients, high expression of SGOL1-AS1 correlates with both pro-inflammatory gene expression and poor survival. Altogether, our data reveal that SGOL1-AS1 is an essential regulator of cell survival in AML cell lines and a possible regulator of pro-inflammatory signaling in AML patients.
Original languageEnglish
Publication statusAccepted/In press - 28 Oct 2022


  • Acute Myeloid Leukemia (AML)
  • long noncoding RNA (lncRNA)
  • inflammatory signaling
  • epigenetic

Research Beacons, Institutes and Platforms

  • Manchester Cancer Research Centre


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