TGIF1 plays a carcinogenic role in esophageal squamous cell carcinoma through the Wnt/ß­catenin and Akt/mTOR signaling pathways.

ABSTRACT

TGFB induced factor homeobox 1 (TGIF1), a transcriptional corepressor, has been reported to be involved in tumorigenesis and cancer development. However, the role of TGIF1 in the growth and metastasis of esophageal cancer is poorly studied. In the present study, it was found that TGIF1 was highly expressed in esophageal cancer tissues and cell lines. The silencing of TGIF1 by siRNA interference significantly inhibited the proliferation, migration, invasion and epithelial­mesenchymal transition (EMT) process of KYSE­150 esophageal cancer cells, and promoted cell apoptosis. Correspondingly, the upregulation of TGIF1 significantly promoted the proliferation and metastatic potential of Eca­109 cells, and reduced apoptosis. Furthermore, the data indicated that the Wnt/ß­catenin and Akt/mammalian target of rapamycin (mTOR) signaling pathways were inhibited by TGIF1 knockdown, and were promoted by the overexpression of TGIF1. It was also confirmed that TGIF1 knockdown reduced tumor growth, inhibited Wnt/ß­catenin and Akt/mTOR pathway activation, and reversed the TGF­ß1­mediated EMT process in a tumor xenograft model. Taken together, the data of the present study suggest that TGIF1 plays an oncogenic role in the progression of esophageal cancer. It may carry out this role by regulating the Wnt/ß­catenin and Akt/mTOR signaling pathways.