9th Annual Symposium
Physics of Cancer
Leipzig, Germany
September 24-26, 2018
Invited Talk
Role of phosphoinositide signaling in mechanoresponse of liver cancer cells
Kalpana Mandal, Paul A. Janmey
University of Pennsylvania, Institute for Medicine and Engineering & Department of Physiology, 1010 Vagelos Research Labs 3340 Smith Walk Philadelphia, PA 19104-6393, USA
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Several cytoskeletal regulators, including talin, ezrin, alpha-actinin, and vinculin, that are activated by tension arising when cells are grown on stiff substrates, are also activated by polyphosphoinositide lipids, in particular PIP2, in the absence of force. These dual mechanisms of activation appear to relate to the finding that some cell types, including the human hepatocellular carcinoma cell Huh7, adopt a phenotype characteristic of adhesion to stiff substrates when they attach to very soft substrates formed by hyaluronic acid (HA) and an integrin ligand such as collagen or fibronectin. Cells that spread on very soft HA-collagen gels exert very low traction stresses compared to cells on stiff 30 kPa substrates, even though cells on both substrates have large spread areas, extensive focal adhesions, and actin bundles. Inhibition of polyphosphoinositide turnover causes Huh7 cells to decrease spreading and detach from HA-collagen substrates, whereas cells on stiffer substrates show almost no response.
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