With a few other papers lined up to be blogged on, my actual research to do, and not enough time to do it all, I’m going to mention this one real quick before I forget about it…
In the July issue of Molecular Biology of the Cell, Shintani et al. have an interesting paper out titled “Phosphoinositide-3 Kinase-Rac1-c-Jun NH2-terminal Kinase Signaling Mediates Collagen I-induced Cell Scattering and Up-Regulation of N-Cadherin Expression in Mouse Mammary Epithelial Cells.”
As much as I’d like to go into detail on what’s in the paper, I’ll just give you the quick run-down: Shintani et al. found that:
- Adhering to Collagen I promotes the reorganization of cell-cell junctional complexes and induces EMT-like changes in E10/NMuMG cells, including increased expression of N-Cadherin and Fibronectin, relocalization of Paxillin to cell periphery as opposed to mature focal adhesions, and enhanced motility. These changes in cell behavior, as well as changes in morphology, were in stark contrast to cells plated on fibronectin.
- Collagen I-induced signaling was mediated by PI3K, but not Src, and occurred through Rac-JNK activation.
- The PI3K-Rac-JNK signaling, and resulting up-regulation of N-Cadherin, were all necessary for the Collagen I-induced EMT-like changes. This signaling pathway was separate from TGFbeta-mediated transformation, and may represent an alternative or concomitant action in cancer progression.
- Phosphoinositide-3 Kinase-Rac1-c-Jun NH2-terminal Kinase Signaling Mediates Collagen I-induced Cell Scattering and Up-Regulation of N-Cadherin Expression in Mouse Mammary Epithelial Cells. Shintani Y, Wheelock MJ, Johnson KR. Mol Biol Cell. 2006 Jul; 17(7):2963-2975. Pubmed.