Heparanase promotes malignant phenotypes of human oral squamous carcinoma cells by regulating the epithelial-mesenchymal transition-related molecules and infiltrated levels of natural killer cells.

These results indicated that knockdown of HPSE suppressed SCC-25 cell proliferation, invasion, migration, and epithelial-mesenchymal transition, possibly via syndecan binding protein and RAB11A, member RAS oncogene family. Moreover, HPSE regulates the infiltrated levels of natural killer cells activated, possibly via DDB1 and CUL4 associated factor 15.