Upregulation of cystatin SN promotes hepatocellular carcinoma progression and predicts a poor prognosis
Autor: | Xirui Liu, Bo Zhang, Yifeng Cui, Jihua Han, Zhaoyang Lu, Lianxin Liu, Fanzheng Meng, Ruipeng Song, Shangha Pan, Hongrui Guo, Yan Wang, Yufeng Liu, Yaliang Lan, Dan Sun, Shugeng Zhang, Shuhang Liang |
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Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Male Carcinoma Hepatocellular Physiology Clinical Biochemistry urologic and male genital diseases Metastasis cystatin SN 03 medical and health sciences Mice Phosphatidylinositol 3-Kinases 0302 clinical medicine Downregulation and upregulation In vivo Cell Movement Original Research Articles Cell Line Tumor medicine Biomarkers Tumor Animals Humans Epithelial–mesenchymal transition Original Research Article PI3K/AKT/mTOR pathway reproductive and urinary physiology Cell Proliferation Gene knockdown epithelial‐mesenchymal transition Chemistry Cell growth Liver Neoplasms Cell Biology hepatocellular carcinoma Neoplasms Experimental Middle Aged medicine.disease Prognosis digestive system diseases female genital diseases and pregnancy complications Up-Regulation Gene Expression Regulation Neoplastic 030104 developmental biology 030220 oncology & carcinogenesis Hepatocellular carcinoma Cancer research Salivary Cystatins Female Proto-Oncogene Proteins c-akt prognostic marker |
Zdroj: | Journal of Cellular Physiology |
ISSN: | 1097-4652 0021-9541 |
Popis: | Cystatin SN, a specific cysteine protease inhibitor, is thought to be involved in various malignant tumors. Therefore, we evaluated the role of cystatin SN in hepatocellular carcinoma (HCC). Notably, cystatin SN was elevated in tumorous samples and cells. Moreover, overexpression of cystatin SN was correlated with tumor diameter and TNM stage. Cox multivariate analysis displayed that cystatin SN was an independent prognosis indicator and that high cystatin SN level was associated with a dismal prognosis. Moreover, cystatin SN enhancement facilitated the proliferation, migratory, and invasive potential of Huh7 and HCCLM3 cells, whereas cystatin SN knockdown caused the opposite effect. Cystatin SN also modulated the epithelial‐mesenchymal transition progression through the PI3K/AKT pathway. In vivo cystatin SN promoted HCCLM3 cell growth and metastasis in xenograft mice model. Thus, cystatin SN was involved in HCC progression and could be a latent target for HCC treatment. |
Databáze: | OpenAIRE |
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