The tumor suppressor kinase LKB1: lessons from mouse models

Research output: Contribution to journalReview ArticleScientificpeer-review

Abstract

Mutations in the tumor suppressor gene LKB1 are important in hereditary Peutz-Jeghers syndrome, as well as in sporadic cancers including lung and cervical cancer. LKB1 is a kinase-activating kinase, and a number of LKB1-dependent phosphorylation cascades regulate fundamental cellular and organismal processes in at least metabolism, polarity, cytoskeleton organization, and proliferation. Conditional targeting approaches are beginning to demonstrate the relevance and specificity of these signaling pathways in development and homeostasis of multiple organs. More than one of the pathways also appear to contribute to tumor growth following Lkb1 deficiencies based on a number of mouse tumor models. Lkb1-dependent activation of AMPK and subsequent inactivation of mammalian target of rapamycin signaling are implicated in several of the models, and other less well characterized pathways are also involved. Conditional targeting studies of Lkb1 also point an important role of LKB1 in epithelial-mesenchymal interactions, significantly expanding knowledge on the relevance of LKB1 in human disease.
Original languageEnglish
JournalJournal of Molecular Cell Biology
Volume3
Issue number6
Pages (from-to)330-340
Number of pages11
ISSN1674-2788
DOIs
Publication statusPublished - 2011
MoE publication typeA2 Review article in a scientific journal

Fields of Science

  • LKB1
  • tumor suppressor
  • mouse model
  • AMPK
  • PEUTZ-JEGHERS-SYNDROME
  • ACTIVATED PROTEIN-KINASE
  • HEMATOPOIETIC STEM-CELLS
  • SKELETAL-MUSCLE
  • NEURONAL POLARIZATION
  • LKB1-DEFICIENT MICE
  • GLUCOSE-HOMEOSTASIS
  • SOMATIC MUTATIONS
  • LKB1-AMPK PATHWAY
  • PROSTATE-CANCER

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