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Microgravity Induces Transient EMT in Human Keratinocytes by Early Down-Regulation of E-Cadherin and Cell-Adhesion Remodeling

Abstract: Changes in cell–matrix and cell-to-cell adhesion patterns are dramatically fostered by
the microgravity exposure of living cells. The modification of adhesion properties could promote
the emergence of a migrating and invasive phenotype. We previously demonstrated that short
exposure to the simulated microgravity of human keratinocytes (HaCaT) promotes an early epithelial–
mesenchymal transition (EMT). Herein, we developed this investigation to verify if the cells maintain

Survival pathways are differently affected by microgravity in normal and cancerous breast cells

Metazoan living cells exposed to microgravity undergo dramatic changes in morphological and biological properties, which ultimately lead to apoptosis and phenotype reprogramming. However, apoptosis can occur at very different rates depending on the experimental model, and in some cases, cells seem to be paradoxically protected from programmed cell death during weightlessness.

Increase in motility and invasiveness of MCF7 cancer cells induced by nicotine is abolished by melatonin through inhibition of ERK phosphorylation

Through activation of the ERK pathway nicotine, in both normal MCF-10A and low malignant breast cancer cells (MCF7), promotes increased motility and invasiveness. Melatonin antagonizes both these effects by inhibiting almost completely ERK phosphorylation. As melatonin has no effect on not-stimulated cells, it is likely that melatonin can counteract ERK-activation only downstream of nicotine-induced activation.

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