The transcription factor 7 like 2-binding protein TIP5 activates β-catenin/transcription factor signaling in hepatocellular carcinoma

Aberrant activation of β-catenin/transcription factor 7 like 2 (TCF7L2) signaling is frequently observed during the progression of hepatocellular carcinoma (HCC). However, regulation of the nuclear β-catenin/TCF7L2 complex remains largely unknown. In the present study, immunoprecipitation and glutathione S-transferase pull-down assays identified transcription termination factor-1 interacting protein 5 (TIP5) as a binding partner of TCF7L2. TIP5 activated β-catenin/TCF7L2 signaling by enhancing the interaction between β-catenin and TCF7L2. The results from quantitative polymerase chain reaction and western blot analysis indicated that TIP5 was upregulated in clinical HCC samples. In addition, TIP5 positively regulated the proliferation of HCC cells in the MTT assay, colony formation in the soft agar assay, migration in the Boyden chamber assay and epithelial-mesenchymal transition of HCC cells by activating β-catenin/TCF7L2 signaling. Therefore, the results of the present study demonstrate that TIP5 serves an oncogenic role in HCC by activating β-catenin/TCF7L2 signaling, suggesting that TIP5 may be a promising therapeutic target for HCC.