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.

中文翻译：

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Sp2通过靶向TRIB3蛋白促进肝细胞癌的侵袭和转移。

目的探讨Sp2在肝细胞癌（HCC）中的生物学功能和分子机制。方法采用组织微阵列免疫组化和蛋白质印迹法研究Sp2在肝细胞组织和邻近非肿瘤组织（ANT）中的表达。在HCC细胞系中，通过CCK8、克隆形成试验、Transwell试验、伤口愈合试验和流式细胞术凋亡分析等体外实验确定了Sp2的作用，并分析了其可能的机制。结果与ANT相比，肝癌组织中Sp2表达显着上调，与肿瘤分期及患者预后不良密切相关。TCGA数据库进一步证实了这些结果。除了，功能研究表明，敲低Sp2不仅会导致细胞增殖减少和细胞凋亡增加，而且还会抑制细胞的迁移和侵袭能力。Sp2沉默可以抑制TRIB3蛋白的表达并下调HCC的内质网应激（ERS）水平。结论 Sp2 可能通过调节 TRIB3 蛋白在促进癌症中发挥作用，这可能是 HCC 的预后因素和潜在的新治疗靶点。