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Comment
. 2014 Oct 27;207(2):167-9.
doi: 10.1083/jcb.201409107.

Ignoring matrix boundaries when the LKB1 master kinase is gone

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Comment

Ignoring matrix boundaries when the LKB1 master kinase is gone

Erik H J Danen. J Cell Biol. .

Abstract

Gradients of soluble attractants as well as extracellular matrix (ECM) proteins serve as cues for directional cell movement. Such "chemotaxis" and "haptotaxis" steers migration of cells during embryonic development, wound healing, and immune responses. In this issue, Chan et al. (2014. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201404067) show that the tumor suppressor LKB1 controls haptotaxis through the microtubule affinity-regulating kinase (MARK) family, one of the many substrates of the LKB1 master kinase. In the absence of this pathway, melanoma cells migrate irrespective of ECM gradients, which may explain the increased metastatic spread observed in LKB1-deficient tumors.

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Figures

Figure 1.
Figure 1.
Summary of known and predicted tumor- and metastasis-suppressing functions of LKB1. (i) Pathways restricted by LKB1 activity are indicated in gray, and pathways promoted by LKB1 are indicated in black. (ii) Using the same color scheme as in i, the effects of LKB1 loss in cancer cells are shown. The resulting known and predicted consequences of LKB1 loss for aspects of tumorigenesis and metastasis are indicated in blue. Note that only a limited subset of LKB1 and AMPK substrates is shown. See the text for further details.

Comment on

References

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