Abnormal sialylation due to overexpression of sialyltransferases has been associated with tumorigenesis and tumor progression. Although ST6Gal-I influences cancer persistence and progression by affecting various receptors, the underlying mechanisms and mediators remain largely obscure, especially in hepatocellular carcinoma (HCC). We found that ST6Gal-I expression was markedly upregulated in HCC tissues and cells, high levels being associated with aggressive phenotype and poor prognosis. Furthermore, we examined the roles and mechanisms of ST6Gal-I in HCC tumorigenesis and metastasis in vitro and in vivo. ST6Gal-I overexpression promoted proliferation, migration and invasion of Huh-7 cells, whereas its knockdown restricted these abilities in MHCC97-H cells. Additionally, in a mouse xenograft model, ST6Gal-I-knockdown MHCC97-H cells formed significantly smaller tumors, implying that ST6Gal-I overexpression can induce HCC cell malignant transformation. Importantly, enhanced HCC tumorigenesis and metastasis by ST6Gal-I may be associated with Wnt/β-catenin signaling promotion, including β-catenin nuclear transition and upregulation of downstream molecules. Together, our results suggest a role for ST6Gal-I in promoting the growth and invasion of HCC cells through the modulation of Wnt/β-catenin signaling molecules, and that ST6Gal-I might be a promising marker for prognosis and therapy of HCC.

The authors have retracted this article [1] because there are errors in some images. In Fig. 2g, a colony picture for Mock group was incorrect. In Fig. 2k, the invasion pictures for Mock and overexpression ST6Gal-1 cells were incorrect. In Fig. 3g, the colony picture for shNC was incorrect. In Fig. 4f, the authors mistakenly provided WB band for GAPDH. In Fig. 4g, the IHC pictures for 10w in Negative Control and DENA-induced Groups were incorrect, and in Fig. 7f, a IHC picture for GSK-3β in DENA-induced Group (10w) was presented incorrectly. Due to these errors the findings are no longer reliable.

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