Increased chromatin plasticity supports enhanced metastatic potential of mouse melanoma cells

- In the B16 melanoma model higher aggressiveness is linked to chromatin decondensation.
- High levels of condensed chromatin reduce the cellular proliferation rate.
- Migration signals induce chromatin condensation in low and high metastatic B16 cells.
- Migration of low and high metastatic B16 cells is dependent on chromatin condensation.

Metastasis formation is strongly dependent on the migration capabilities of tumor cells. Recently it has become apparent that nuclear structure and morphology affect the cellular ability to migrate. Previously we found that migration of melanoma cells is both associated with and dependent on global chromatin condensation. Therefore, we anticipated that tumor progression would be associated with increased chromatin condensation. Interestingly, the opposite has been reported for melanoma. In trying to resolve this contradiction, we show that during growth conditions, tumor progression is associated with global chromatin de-condensation that is beneficial for faster proliferation. However, upon induction of migration, in both low- and high-metastatic mouse melanoma cells chromatin undergoes condensation to support cell migration.Our results reveal that throughout tumor progression induction of chromatin condensation by migration signals is maintained, whereas the organization of chromatin during growth conditions is altered. Thus, tumor progression is associated with an increase in chromatin dynamics.