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Breast  cancer is a common cancer in women, with a highly variable course, from  inoffensive to lethal. To find a more effective strategy for its treatment,  sodium valproate has been tested as an anti-cancer drug; it is the only  clinically available histone deacetylase inhibitor. However, data about the  effects of sodium valproate on breast cancer are insufficient in both animals  and humans; studies have yielded conflicting conclusions. In particular, little  is known about the association between expression of the metastasis suppressor Nm23H1 gene and breast cancer. We hypothesized that sodium valproate regulates  NM23H1 expression, and affects migration and/or invasion. We found that sodium  valproate at concentrations of 0.8-3.2 mM inhibits migration and modulates Nm23H1 gene expression in a concentration-dependent manner. Confluent MDA-MB-231  cells were scratched by a micropipette tip after VPA treatment for 24 h; 24 h  later, the scratch was almostly closed in the 0 mM VPA-treated cells, while the  3.2 mM VPA-treated cells migrated the slowest. The cell migration ratio exposed  to 0.8, 1.6 and 3.2 mM VPA was about 66.67, 30.67 and 26.67% (P &lt; 0.05). We  also found evidence that sodium valproate upregulates NM23H1 expression, which  is a clue to its anti-cancer mode of action. The NM23H1 gene expression  was relative fold increased determined by Western blotting at 3.2 mM VPA.  Collectively, these observations indicate that sodium valproate has potential  for use in breast cancer treatment.

Sodium valproate inhibits MDA-MB-231 breast cancer cell migration by upregulating NM23H1 expression