Upregulated SSB Is Involved in Hepatocellular Carcinoma Progression and Metastasis through the Epithelial-Mesenchymal Transition, Antiapoptosis, and Altered ROS Level Pathway

Author:

Wu Hao1ORCID,Zhang Zhixin1ORCID,Han Xinyu2,Zhang Sai3ORCID,Zhang Jinrui1ORCID,Han Pinsheng1,Zhang Youcheng1,Bai Yi4,Zhang Yamin4ORCID

Affiliation:

1. The First Central Clinical School, Tianjin Medical University, Tianjin 300070, China

2. Department of Genetics, School of Basic Medical, Tianjin Medical University, Tianjin 300070, China

3. School of Medicine, Nankai University, Tianjin 300192, China

4. Department of Hepatobiliary Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin 300192, China

Abstract

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors with high morbidity and mortality. Therefore, finding new diagnostic and therapeutic targets is vital for HCC patients. Recent studies have shown that dysregulation of RNA-binding proteins is often associated with cancer progression. Several studies have reported that the RNA-binding protein SSB can promote cancer occurrence and progression and is linked to tumor epithelial-mesenchymal transition (EMT), which could be a new diagnostic marker and therapeutic target. However, the expression and function of SSB in HCC remain to be elucidated. Therefore, this study is aimed at clarifying the expression and biological function of SSB in HCC through bioinformatics analysis combined with in vitro experiments. We found that SSB is highly expressed in HCC and is associated with the poor prognosis of HCC patients, and it can serve as an independent unfavorable prognostic factor. Knockdown of SSB can inhibit the growth of HCC cells in vitro, increase the level of apoptosis and the expression of pro-apoptosis-related proteins, and decrease the expression of antiapoptotic proteins. Meanwhile, SSB knockdown reduced HCC cell invasiveness, and the expression of EMT-related proteins changed significantly. We also found that the gene SSB was associated with the level of oxidative stress in liver cancer cells, and the level of intracellular reactive oxygen species (ROS) increased after knockdown of SSB. The results of bioinformatics analysis also showed that high expression of SSB may affect the effect of checkpoint blockade (ICB) therapy. In conclusion, we found that SSB is highly expressed in HCC and that upregulated SSB can promote the proliferation and metastasis of HCC through antiapoptotic, altered intracellular oxidative stress level, and EMT pathways, which can serve as a new diagnostic marker and therapeutic target, and patients with high SSB expression may not have obvious ICB therapy effect.

Funder

Tianjin Health Science and Technology Project

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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