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
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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