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AB STRACTThe fluorescence polarization anisotropies of ethidium intercalated in duplex DNAs containing 12 to 60 bp were measured and analyzed using a theory of deformable rods to obtain their hydrodynamic radii (RH). The apparent RH 5 10.0 0.2 A for 12 and 24 bp, but increases to 1 1 .5-12.0 A between 40 and 60 bp. This variation in RH is attributed to the presence of slowly relaxing bends in the DNA.Consequently, the static equilibrium persistence length must be much smaller than the dynamic persistence length ('d) defined by the dynamic (instantaneous) bending rigidity. We estimate that d A. RH of a 48 bp duplex DNA is largely independent of NaCl concentration, which suggests that interionic forces do not much affect the rotational friction. However, RH depends significantly on the concentrations of other ions, especially Mg2 and Mn2, which are believedto affect the hydration of DNA.

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The tetraspanin and tumor suppressor KAI1 is downregulated or lost in many cancers which correlates with poor prognosis. KAI1 acts via physical/functional crosstalk with other membrane receptors. Also, a splice variant of KAI1 (KAI1-SP) has been identified indicative of poor prognosis. We here characterized differential effects of the two KAI1 variants on tumor biological events involving integrin (αvß3) and/or epidermal growth factor receptor (EGF-R). In MDA-MB-231 and -435 breast cancer cells, differential effects were documented on the expression levels of the tumor biologically relevant integrin αvß3 which colocalized with KAI1-WT but not with KAI1-SP. Cellular motility was assessed by video image processing, including motion detection and vector analysis for the quantification and visualization of cell motion parameters. In MDA-MB-231 cells, KAI1-SP provoked a quicker wound gap closure and higher closure rates than KAI1-WT, also reflected by different velocities and average motion amplitudes of singular cells. KAI1-SP induced highest cell motion adjacent to the wound gap borders, whereas in MDA-MB-435 cells a comparable induction of both KAI1 variants was noticed. Moreover, while KAI1-WT reduced cell growth, KAI1-SP significantly increased it going along with a pronounced EGF-R upregulation. KAI1-SP-induced cell migration and proliferation was accompanied by the activation of the focal adhesion and Src kinase. Our findings suggest that splicing of KAI1 does not only abrogate its tumor suppressive functions, but even more, promotes tumor biological effects in favor of cancer progression and metastasis.

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