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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
Summary
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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