SSR3 and SEC61G co-expression promotes proliferation in hepatocellular carcinoma cells

Abstract BACKGROUND Hepatocellular carcinoma (HCC) is a malignant tumor with a high incidence and poor prognosis. With the use of bioinformatics and next-generation sequencing technology, several molecular markers related to HCC diagnosis, treatment, and aetiology have been found. As an example, the upregulation of signal sequence receptor 3 (SSR3) has been linked to tumorigenesis. Studies also suggest that overexpression of SSR3 predicts poor survival in patients with HCC. However, research on the function and genes co-expressed with SSR3 is limited. METHODS The interaction between SSR3 and SEC61G proteins was analyzed using the STRING database. Correlation analysis of SSR3 and SEC61G mRNA levels was performed using the cBioPortal database. Expression levels of these two genes in HCC and normal tissues were evaluated, and the relationship with prognosis was analysed using the UALCAN database and tumor tissues obtained from surgical resection. Small interfering RNA targeting SSR3 or SEC61G , and overexpression vectors of SSR3 or SEC61G were transfected into HCC cells. SSR3 and SEC61G mRNA levels were detected using quantitative polymerase chain reaction, and a CCK-8 assay was performed to determine cell proliferation. RESULTS SSR3 and SEC61G mRNA levels were positively correlated (Spearman: 0.42, P ˂ 0.001), and the expression was increased in HCC tissues compared to that in normal tissues ( P < 0.05). SSR3 knockdown decreased SEC61G mRNA levels. In contrast, SSR3 overexpression increased SEC61G mRNA levels. Higher SSR3 and SEC61G mRNA levels were associated with shorter overall survival ( P < 0.01) and higher clinical stages ( P < 0.05) in patients with HCC. Moreover, SSR3 and SEC61G co-expression promoted HCC cell proliferation ( P < 0.01). CONCLUSION SSR3 co-expressed with SEC61G facilitated the proliferation of HCC cells and was associated with poor prognosis in patients with HCC.