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KRAS induces lung tumorigenesis through microRNAs modulation

Lei Shi1,2, Justin Middleton3, Young-Jun Jeon3

  • 1Transcriptional Networks in Lung Cancer Group, Cancer Research UK Manchester Institute, The University of Manchester, Wilmslow Road, Manchester, M20 4BX, UK.

Cell Death & Disease
|February 15, 2018
PubMed

Insights

Oncogenic KRAS upregulates miR-30c and miR-21 in non-small cell lung cancer (NSCLC), promoting drug resistance and tumor growth. These microRNAs (miRNAs) are potential early biomarkers and therapeutic targets for NSCLC.

Area of Science:

  • Molecular Oncology
  • Cancer Biology
  • Biochemistry

Background:

  • Oncogenic KRAS is a key driver in non-small cell lung cancer (NSCLC) pathogenesis.
  • MicroRNAs (miRNAs) are critical regulators of gene expression implicated in tumorigenesis.
  • Understanding KRAS-mediated miRNA regulation is essential for NSCLC treatment.

Purpose of the Study:

  • To investigate the role of KRAS-regulated miRNAs in NSCLC.
  • To identify potential diagnostic biomarkers and therapeutic targets for NSCLC.

Main Methods:

  • Overexpression of wild type and mutant KRAS (KRASG12D) in human and mouse cell lines.
  • Analysis of miRNA expression profiles in NSCLC cells and patient samples.
  • In vivo studies using a mouse model of lung cancer and systemic delivery of anti-miRNA oligonucleotides.
  • Mechanistic studies involving transcription factor binding assays.

Main Results:

  • KRAS isoforms upregulate miR-30c and miR-21, which inhibit tumor suppressor genes (NF1, RASA1, BID, RASSF8), enhancing drug resistance and cell migration/invasion.
  • Elevated miR-30c and miR-21 levels were observed in early-stage NSCLC tumors and plasma compared to normal lung tissue.
  • Systemic delivery of LNA-anti-miR-21 combined with cisplatin suppressed lung tumor development in mice.
  • ELK1 was identified as a transcriptional activator of miR-30c and miR-21.

Conclusions:

  • miR-30c and miR-21 are oncogenic drivers in NSCLC, acting as potential biomarkers for early detection.
  • Targeting miR-30c and miR-21 through silencing offers a promising therapeutic strategy for NSCLC.

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