Both enforced expression of miR-338-3p and small interfering RNA induced Rab14-mediated accumulation of N-cadherin in the cell -cell junctions or Hhat-associated matrix metalloproteinase (MMP) degradation, which may underline the metastasis defects caused by loss of miR-338-3p in GC.
In conclusion, this study provides a new evidence on that Rab14 functions as a novel tumor oncogene and could be a potential therapeutic target in gastric cancer.
Furthermore, the reintroduction of RAB14 partially abrogated the miR-320a-mediated downregulation of RAB14 and rescued the miR-320a-induced effects on GC cell growth.