9th Annual Symposium
Physics of Cancer
Leipzig, Germany
September 24-26, 2018
Contributed Talk
Biomechanics of glioblastoma cells by atomic force microscopy
Tomasz Zieliński1, Joanna Zemla1, Klaudia Suchy1, Joanna Pera2, Małgorzata Lekka1
1Polish Academy of Sciences, Institute of Nuclear Physics, Department of Biophysical Microstructures, Radzikowskiego 152, PL-31342, Kraków, Poland
2Jagiellonian University, Department of Neurology, Botaniczna 3, PL-31503, Kraków, Poland
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Glioblastoma is a one of most deadly cancers, thus, understanding mechanisms governing its invasion is important for the development of novel treatment approaches. Nanomechanics of living cells is one of essential cues shown to play a role in glioblastoma migration and metastasis[1], [2]. Various studies, carried so far, have shown that the main structure responsible for mechanical properties of cells is a cytoskeleton, in particular, actin filaments [3], [4].
In our studies, we focused on nanomechanical properties of glioblastoma cells in relation to changes induced in actin filament organization upon cytochalasin D treatment. Two cell lines with distinct morphologies were chosen, namely, U118 and U138 possessing fibroblast and keratinocyte-like characteristics, respectively. Elastic properties of cells (quantified through the Young’s modulus, [4]) and F-actin organization in cells were obtained by applying atomic force and fluorescence microscopes. Results identify that these glioblastoma response to cytochalasin D (5µg/ml) in a time(dose)-dependent manner resulted in both softening and stiffening of cells. Fibroblasts-like cells (U118) increase their deformability (Young’s modulus decreases) after 10 minutes of cytochalasin D incubation. As Young’s modulus decreases for all probed indentations (from 200 nm to 800 nm), softening of cells, we can postulate that cytochalasin D re-organization proceeds within a whole actin filament network. Keratinocyte-like U138 cells respond differently. For the same incubation time, there was no changes in elastic properties while increasing the time of cytochalasin D exposure to 30 minutes induced stiffening of these cells. They become more rigid within a whole indentation depth. These finding are analogous to that recently published showing pronounced effect of cytochalasin D on fibroblasts and no effect for keratinocytes [5]. Summarizing, the fact that U118 glioblastoma cells are stiffer than U138 ones can be explained by well-differentiated network of actin filaments with the presence of stress fibres in U118 and lack of them in U138. Exposure to cytochalasin D shows that elastic properties of fibroblast-like U118 are govern by actin filaments while their role in deformability of U138 is less significant.
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