A further mechanistic study revealed that forkhead box D3 (FOXD3) was a direct target of miR‑425‑5p, and gain‑ and loss‑of‑function of FOXD3 studies demonstrated that FOXD3 suppressed HCC cell proliferation, migration, and invasion.
In vitro and in vivo functional results showed that ectopic FOXD3 inhibited the proliferation, migration, epithelial-mesenchymal transition (EMT) and invasion in HepG2 and SMMC-7721 cells, and FOXD3 depletion in HepG2 and QGY-7701 cells showed the adverse effects (p<0.05).
Depletion of FOXD3 expression promotes breast cancer cell proliferation and invasion in vitro, whereas overexpression of FOXD3 inhibits breast cancer cell proliferation and invasion both in vitro and in vivo.
FOXD3 is downregulated during the migration of the melanocyte lineage from the neural crest, and our previous work supports a role for FOXD3 in suppressing melanoma cell migration and invasion.
These data show that FOXD3 expression downregulates migration and invasion in melanoma cells and Rnd3, a target known to be involved in these properties.