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A KRAS-responsive long non-coding RNA controls microRNA processing

Lei Shi1,2, Peter Magee1,2, Matteo Fassan3

  • 1Transcriptional Networks in Lung Cancer Group, Cancer Research UK Manchester Institute, University of Manchester, Manchester, UK.

Nature Communications
|April 2, 2021
PubMed

Insights

Wild-type KRAS (KRASWT) amplification drives lung cancer. Researchers found KIMAT1, a KRAS-responsive lncRNA, promotes tumorigenesis by regulating microRNAs, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Wild-type KRAS (KRASWT) amplification is linked to poor survival in cancer.
  • The role of KRASWT overexpression in lung cancer progression remains unclear.

Purpose of the Study:

  • To identify and characterize a KRAS-responsive long non-coding RNA (lncRNA) in lung cancer.
  • To elucidate the mechanism by which this lncRNA influences lung tumorigenesis.

Main Methods:

  • Correlation analysis of KIMAT1 and KRAS levels in cell lines and patient specimens.
  • Investigated KIMAT1's role in microRNA processing and biogenesis.
  • Assessed the impact of KIMAT1 knockdown on KRAS signaling and tumor growth in vitro and in vivo.

Main Results:

  • Identified KIMAT1 (ENSG00000228709) as a KRAS-responsive lncRNA correlating with KRAS levels.
  • KIMAT1, a MYC target, stabilizes DHX9 and NPM1 to promote oncogenic miRNA processing.
  • KIMAT1 silences p21, halting tumor suppressor miRNA biogenesis, and KRAS downstream signaling.

Conclusions:

  • KIMAT1 sustains KRAS signaling through a positive feedback loop in lung cancer progression.
  • KIMAT1 knockdown inhibits KRAS expression and downstream signaling, arresting tumor growth.
  • Targeting KIMAT1 presents a potential strategy to combat KRAS-driven lung tumorigenesis.

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