Perturbations in cancer cell deformability and resistance to shear forces.
During hematogenous metastasis, circulating cancer cells appear to be killed in the microcirculation by a non-exclusive mechanism, involving the mechanical trauma consequent upon cancer cell interactions with the vessel wall. Various observations by others indicate that with increased cell deformability, there is decreased intravascular cell killing. We have therefore critically examined the effects of agents previously shown to modify cell deformability, on the susceptibility of Ehrlich ascites tumor and L1210 leukemia cells to mechanical damage on passage through polycarbonate membranes in vitro. Treatment with neuraminidase, trypsin or EGTA, was previously shown to increase cell deformability. However, in the present studies, neuraminidase treatment was associated with increased cell loss on filtration; trypsin treatment with small decreases in cell loss, and EGTA treatment with decreased loss. Consideration of the effects of these agents on cell deformability and membrane strength suggests that under the described experimental conditions, the latter appears more important for survival than the former. As proteolytic and glycolytic enzymes and calcium ions are involved in the release of cancer cells from tumors and invasive events, the effects described here may be relevant to the variability of cancer cells with respect to the metastatic process.
D000818:Animals; D002286:Carcinoma, Ehrlich Tumor; D002465:Cell Movement / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D004533:Egtazic Acid / Q000494:pharmacology; D005374:Filtration; D006801:Humans; D007939:Leukemia L1210; D009362:Neoplasm Metastasis; D009439:Neuraminidase / Q000494:pharmacology; D014357:Trypsin / Q000494:pharmacology
D004533:Egtazic Acid; D009439:Neuraminidase; D014357:Trypsin