DEAH-box polypeptide 32 promotes hepatocellular carcinoma progression via activating the β-catenin pathway

Purpose Hepatocellular carcinoma (HCC) is refractory cancer with high morbidity and high mortality. DEAH-box polypeptide 32 (DHX32) was upregulated in several types of malignancies and predicted poor prognosis. Herein, we investigated the role of DHX32 in HCC progression. Methods The expression of DHX32, beta-catenin, and epithelial-mesenchymal transition (EMT)-related makers were determined by Western blot and quantitative real-time PCR assays. Cell proliferation was tested by EdU cell proliferation assay. The effect of DHX32 and beta-catenin on cell migration and invasion were detected by wound-healing and Traswell invasion assays. Tumour xenografts were performed to determine the effect of DHX32 on HCC tumour growth. Results High level of DHX32 expression was associated with reduced overall survival in HCC patients. DHX32 expression was upregulated in human HCC cells and ectopic expression of DHX32 induced EMT, promoted the mobility and proliferation of HCC cells, and enhanced tumour growth in vivo. Silencing DHX32 reversed EMT, inhibited the malignancy behaviors of HCC cells, and suppressed tumour growth. Mechanistically, silencing DHX32 decreased the expression of beta-cateninin in nucleus and beta-catenin siRNA abrogated DHX32-mediated HCC progression. Conclusion DHX32 was an attractive regulator of HCC progression and indicated DHX32 canserve as a potential biomarker and therapeutic target for HCC patients.

Automated summary

High expression of DHX32 is associated with reduced overall survival in HCC patients. DHX32 upregulation induces EMT, promotes mobility and proliferation of HCC cells, and enhances tumor growth in vivo. Silencing DHX32 reverses EMT, inhibits malignancy behaviors of HCC cells, and suppresses tumor growth.