These data suggested that HtrA1 as an inhibitor in gastric cancer cells resulted in anti-proliferation, reduced invasion, decreased migration, and suppressed growth and may be an effective molecular targets on gastric cancer treatment.
Reduction of HtrA1 levels resulted in the epithelial-to-mesenchymal transition with acquisition of mesenchymal phenotypic characteristics, including increased growth rate, migration, and invasion, as well as expression of mesenchymal biomarkers.
Loss of HtrA1 was more frequently found in tumors in Edmondson grade III-IV, especially in those with venous invasion, compared to tumors in Edmondson grade I-II.