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The interfacial charge formation of self-assembled monolayers (SAMs) of thiol derivatives on gold was investigated by streaming potential and streaming current measurements in aqueous electrolyte solutions. All experiments were performed at a slit channel formed by two parallel sample plates. For the first time, ζ potentials of planar SAM−solution interfaces were determined experimentally. Surface pK values were calculated from the pH dependence of the ζ potential. Monolayers carrying ω-carboxylic moieties show a shift of the pK toward the alkaline direction as compared to the carboxy-terminated alkanethiol molecules in solution. Contact angle titrations using a captive bubble method confirmed the dissociation behavior of monolayers with acidic groups. Monolayers of methyl-terminated thiols exhibit ζ potential−pH plots that account for unsymmetrical ion adsorption. Models of the electric double layer are discussed to describe the interface between self-assembled monolayers and electrolyte solutions. Two contrary situations were found depending on the process which generates surface charges. For methyl-functionalized SAMs, the main part of the surface charge is compensated within the diffuse double layer. In contrast, at monolayer surfaces bearing carboxylic acid groups, the main part of the countercharge was found to be located in the stagnant part of the double layer.

To undergo mitosis successfully, most animal cells need to acquire a round shape to provide space for the mitotic spindle. This mitotic rounding relies on mechanical deformation of surrounding tissue and is driven by forces emanating from actomyosin contractility. Cancer cells are able to maintain successful mitosis in mechanically challenging environments such as the increasingly crowded environment of a growing tumor, thus, suggesting an enhanced ability of mitotic rounding in cancer. Here, it is shown that the epithelial-mesenchymal transition (EMT), a hallmark of cancer progression and metastasis, gives rise to cell-mechanical changes in breast epithelial cells. These changes are opposite in interphase and mitosis and correspond to an enhanced mitotic rounding strength. Furthermore, it is shown that cell-mechanical changes correlate with a strong EMT-induced change in the activity of Rho GTPases RhoA and Rac1. Accordingly, it is found that Rac1 inhibition rescues the EMT-induced cortex-mechanical phenotype. The findings hint at a new role of EMT in successful mitotic rounding and division in mechanically confined environments such as a growing tumor.

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