TACC3 promotes gastric carcinogenesis by promoting epithelial-mesenchymal transition through the ERK/Akt/cyclin D1 signaling pathway

Abstract

Background/Aim: The present study investigated the oncogenic functions of TACC3 in the progression of gastric cancer (GC). Materials and Methods: We analysed TACC3 in relation to cell growth, invasion capability, expression of epithelial-mesenchymal transition (EMT)- related markers, and ERK/Akt/cyclin D1 signaling factors. The correlation between the immunohistochemically confirmed expression of TACC3 and clinical factors was also analyzed. Results: The increased proliferation and invasion of TACC3-over-expressing GC cells was accompanied by altered regulation of EMT-associated markers and activation of ERK/Akt/cyclin D1 signaling. Immunohistochemical analysis of TACC3 in human GC tissues revealed that its expression is correlated with aggressive characteristics and poor prognosis of intestinal-type GC. Conclusion: TACC3 contributes to gastric tumorigenesis by promoting EMT via the ERK/Akt/cyclin D1 signaling pathway. The correlation between TACC3 expression and multiple clinicopathological variables implies that its effective therapeutic targeting in GC will depend on the tumor subtype. © 2021 International Institute of Anticancer Research. All rights reserved.