DIAPH3 promoted the growth, migration and metastasis of hepatocellular carcinoma cells by activating beta-catenin/TCF signaling

• DOI: 10.1007/s11010-017-3125-7
• Publication Date: 2017-08-09T10:00:50Z
• Authors: Li Dong; Zhijun Li; Liying Xue; Gang Li; Cuiying Zhang; Zhihui Cai; Hui Li; Ruifang Guo
• Keywords: 0303 health sciences; Carcinoma, Hepatocellular; Liver Neoplasms; Formins; Hep G2 Cells; Neoplasm Proteins; 3. Good health; 03 medical and health sciences; Cell Movement; Humans; Neoplasm Metastasis; TCF Transcription Factors; beta Catenin; Adaptor Proteins, Signal Transducing

The enhanced ability of cancer cell migration and metastasis is the major cause for the cancer-related death of hepatocellular carcinoma (HCC). Better understanding the mechanisms for the motility of cancer cells will benefit the treatment. Diaphanous-related formin 3 (DIAPH3) has been reported to regulate the motility of cells by remodeling the cytoskeleton. However, the mechanism through which DIAPH3 regulated the motility of cancer cells remains largely unknown. In this study, we have shown that the expression of DIAPH3 was up-regulated in HCC. DIAPH3 positively regulated the growth, migration, colony formation, epithelia mesenchymal transition, and metastasis of HCC cells. Mechanically, DIAPH3 activated the beta-catenin/TCF signaling by binding HSP90 and disrupting the interaction between GSK3beta and HSP90. Taken together, our study demonstrated the oncogenic activity of DIAPH3 in the progression of HCC and suggested that PDIAPH3 might be a therapeutic target.