Focal Adhesion Kinase Functions as an Akt Downstream Target in Migration of Colorectal Cancer Cells

We show that all three kinases can be found in one protein complex; the interaction between Akt and Src is indirect and mediated by focal adhesions kinase

Jolana Turečková; Martina Vojtěchová; Michaela Krausová; Eva Šloncová; Vladimír Korínek

2014

Scholarcy highlights

  • Cancer metastasis results from progression of a tumor in situ to an invasive tumor involving the acquisition of cell motility mediated by changes in the cytoskeleton, loss of cell-cell adhesion, and gain of cellmatrix adhesion along with production and activation of extracellular proteases
  • We show that focal adhesions kinase is a downstream target for Akt and that the Akt-induced phosphorylation of FAK partly depends on Src
  • Protein G-Sepharose 4 Fast Glow was purchased from Amersham Biosciences, Fugene was from Roche, 4-OH-hydroxytamoxifen was from Sigma, and puromycin and G418 were from Alexis
  • FAK, and Src Are Involved in Migration of Colorectal Cancer Cells
  • The same situation occurred when the cells were treated with the Src inhibitor SU6656 as well as when the experiments were performed with the cells lacking FAK
  • Induction of iAkt was accompanied by an approximately 50% increase of phosphorylation of FAK in the DLD/GIPZ control cells
  • To see whether the inhibitors do not interfere with the proliferation status of the cells, immunohistochemical staining was used with antibody against proliferating cell nuclear antigen, one of the markers expressed in proliferating cells
  • This Akt promigratory role is partly dependent on active Src. Besides migration, focal adhesions kinase, Akt, Src, and PI3 kinases are involved in invasion, but their interactions in this process are less clear and will certainly need additional evaluation

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