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Updated: Feb 21, 2026

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Aurora-A-mediated phosphorylation of LKB1 compromises LKB1/AMPK signaling axis to facilitate NSCLC growth and

X Zheng1, J Chi1, J Zhi1

  • 1Department of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Oncology Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center of Cancer, Tianjin, China.

Oncogene
|October 3, 2017
PubMed

Insights

Aurora kinase A (AURKA) phosphorylates LKB1, disrupting the LKB1/AMPK pathway and promoting non-small cell lung cancer (NSCLC) growth. Targeting AURKA may offer a new therapeutic strategy for NSCLC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Loss-of-function mutations in LKB1 are common in non-small cell lung cancers (NSCLCs), driving tumor initiation and progression.
  • The upstream regulators of LKB1 activation and function in NSCLC remain largely uncharacterized.

Purpose of the Study:

  • To investigate the upstream signaling pathways that regulate LKB1 activity in NSCLC.
  • To elucidate the role of Aurora kinase A (AURKA) in LKB1 function and its impact on NSCLC pathogenesis.

Main Methods:

  • Investigated the interaction and phosphorylation of LKB1 by AURKA using molecular biology techniques.
  • Assessed the functional consequences of AURKA-mediated LKB1 phosphorylation on NSCLC cell proliferation, invasion, and migration.
  • Analyzed AURKA expression levels and their correlation with patient outcomes in NSCLC cohorts.

Main Results:

  • Demonstrated that AURKA phosphorylates LKB1, leading to compromised LKB1/AMPK signaling.
  • Showed that AURKA-mediated LKB1 phosphorylation enhances NSCLC cell proliferation, invasion, and migration.
  • Found elevated AURKA levels in NSCLC patients, correlating with poorer prognoses, particularly in lung adenocarcinoma.

Conclusions:

  • AURKA-mediated phosphorylation of LKB1 impairs the LKB1/AMPK pathway, contributing to NSCLC development.
  • AURKA activation drives NSCLC progression by disrupting energy metabolism and promoting tumorigenesis.
  • AURKA represents a potential therapeutic target for NSCLC driven by its hyperactivity.

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