Sp2 promotes invasion and metastasis of hepatocellular carcinoma by targeting TRIB3 protein.

OBJECTIVE

To explore the biological function and molecular mechanism of Sp2 in hepatocellular carcinoma (HCC).

METHODS

Tissue microarray immunohistochemistry and western blot were used to study the expression of Sp2 in hepatocellular tissue and adjacent non-neoplastic tissues (ANT). In HCC cell lines, the role of Sp2 was determined by in vitro experiments such as CCK8, clone formation test, Transwell assay, wound-healing assay, and flow cytometry apoptotic analysis, and its possible mechanism was analyzed.

RESULTS

Compared with ANT, Sp2 expression in HCC tissues was significantly up-regulated, which was strongly associated with stage of tumor and poor prognosis of patients. TCGA database were further confirmed these results. Besides, functional studies had shown that Sp2 knockdown not only leads to a decrease in cell proliferation and an increase in cell apoptosis but also inhibits the cells' abilities of migration and invasion. Sp2 silencing could inhibit the expression of TRIB3 protein and down-regulate the endoplasmic reticulum stress (ERS) level of HCC.

CONCLUSION

Sp2 may play a part in promoting cancer by regulating TRIB3 protein, which may be a factor of prognostic and a potential new therapeutic target for HCC.