SSNA1 Promotes Hepatocellular Carcinoma Metastasis Via STAT3/EMT Induction

Background/Aim: Hepatocellular carcinoma (HCC) currently represents the third most prevalent cause of cancer related deaths globally. HCC is typically diagnosed at advanced stages with metastasis, and has a poor outcome. In order to identify useful biomarkers for early diagnosis and develop novel therapeutic targets, it is necessary to better understand the cellular mechanisms driving HCC progression. Materials and Methods: Public datasets were used to detect Sjogren's syndrome nuclear autoantigen-1 (SSNA1) expression in HCC. Scratch assay and transwell invasion assays were used to evaluate the migration and invasion ability of HCC cells. We explored the molecular mechanism by western blotting, viability and transfection assays. Results: SSNA1 was found up-regulated in human HCC tissues. SSNA1 expression increased along with HCC progression. In addition, elevated SSNA1 expression in HCC patients was closely correlated to a poor prognosis. The proliferation and apoptosis of HCC cells were unaffected by reducing SSNA1 expression. Meanwhile, STAT3/EMT axis inhibition mediated by SSNA1 depletion prevented HCC cells from migrating and invading in vitro. Conclusion: SSNA1 could be used as a biomarker for HCC diagnosis and prognosis, and point the direction for the future investigation of innovative approaches to target and treat HCC.

Automated summary

Hepatocellular carcinoma (HCC) is the third leading cause of cancer related deaths worldwide. Understanding the cellular mechanisms driving HCC progression is crucial for early diagnosis and the development of novel therapeutic targets. SSNA1 expression was found to be up-regulated in HCC tissues and correlated with poor prognosis. Inhibition of the STAT3/EMT axis mediated by SSNA1 depletion prevented HCC cells from migrating and invading in vitro.