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LKB1 inhibits HPV-associated cancer progression by targeting cellular metabolism

Q Zeng1,2, J Chen2, Y Li2

  • 1Key Laboratory of Pathobiology, Ministry of Education, Norman Bethune College of Medicine, Jilin University, Changchun, China.

Oncogene
|August 23, 2016
PubMed

Insights

Liver kinase B1 (LKB1) loss promotes cancer growth and metastasis in human papillomavirus (HPV)-associated cancers by increasing glycolysis. Restoring LKB1 can inhibit tumor progression, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Metabolic Pathways

Background:

  • Liver kinase B1 (LKB1) is frequently inactivated in various cancers, including human papillomavirus (HPV)-associated cervical cancer.
  • The specific role of LKB1 mutations in cervical cancer initiation and progression remains largely unexplored.

Purpose of the Study:

  • To investigate the functional significance of LKB1 inactivation in HPV-associated cervical cancer.
  • To elucidate the impact of LKB1 on cellular metabolism, proliferation, and metastasis in the context of HPV infection.

Main Methods:

  • Utilized mouse embryonic fibroblasts and HPV-transformed cells with LKB1 manipulation (knockdown/ectopic expression).
  • Employed tumorigenesis and lung metastasis models in syngeneic mice.
  • Analyzed glycolytic pathway enzymes, including hexokinase-II (HK-II), and c-MYC expression.
  • Examined LKB1 and HK-II expression in normal and HPV-associated cervical lesions.

Main Results:

  • LKB1 loss combined with HPV16 E6/E7 expression promoted cell proliferation and aerobic glycolysis while suppressing senescence.
  • LKB1 deficiency enhanced glycolysis, anchorage-independent growth, migration, and invasion in HPV-transformed cells.
  • LKB1 depletion significantly increased lung metastasis in vivo, and HPV16 E6/E7 upregulated HK-II via c-MYC, a process reversed by LKB1 reintroduction.

Conclusions:

  • LKB1 functions as a tumor suppressor by inhibiting HPV-driven aerobic glycolysis and progression.
  • The inverse correlation between LKB1 and HK-II in cervical lesions highlights LKB1's role in metabolic regulation.
  • Targeting cellular metabolism, specifically LKB1-mediated pathways, presents a potential therapeutic strategy for HPV-associated malignancies.

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