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The CREB coactivator CRTC2 promotes oncogenesis in LKB1-mutant non-small cell lung cancer

Laura Rodón1, Robert U Svensson2, Ezra Wiater1

  • 1Peptide Biology Laboratories, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.

Science Advances
|July 30, 2019
PubMed

Insights

Loss of LKB1 in lung cancer activates CRTC2, promoting tumor growth via ID1. Inhibiting CRTC2 and ID1 may offer new non-small cell lung cancer (NSCLC) therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • The LKB1 tumor suppressor is frequently inactivated in non-small cell lung cancer (NSCLC).
  • LKB1 normally activates AMPK family kinases, including SIKs, which regulate gene expression through CRTC coactivators.
  • Loss of LKB1 leads to SIK inactivation, CRTC activation, and increased expression of CREB target genes.

Purpose of the Study:

  • To investigate the role of CRTC2 in LKB1-deficient NSCLC.
  • To identify therapeutic targets for LKB1-mutant NSCLC.

Main Methods:

  • Analysis of CRTC2 activity in LKB1-mutant NSCLC cells.
  • Assessment of CRTC2's role in tumor growth.
  • Evaluation of ID1 as a downstream target of CRTC2.

Main Results:

  • CRTC2 is constitutively active (unphosphorylated) in LKB1-mutant NSCLC.
  • Activated CRTC2 drives tumor growth, partly by up-regulating the CREB target gene ID1.
  • Elevated ID1 expression correlates with poor prognosis in LKB1-deficient NSCLC.

Conclusions:

  • CRTC2 is a key driver in LKB1-deficient NSCLC.
  • Targeting CRTC2 and its downstream effector ID1 may represent a promising therapeutic strategy for NSCLC patients with LKB1 mutations.

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