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Upregulation of cystatin SN promotes hepatocellular carcinoma progression and predicts a poor prognosis
Author(s) -
Cui Yifeng,
Sun Dan,
Song Ruipeng,
Zhang Shugeng,
Liu Xirui,
Wang Yan,
Meng Fanzheng,
Lan Yaliang,
Han Jihua,
Pan Shangha,
Liang Shuhang,
Zhang Bo,
Guo Hongrui,
Liu Yufeng,
Lu Zhaoyang,
Liu Lianxin
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28828
Subject(s) - cystatin c , cystatin , hepatocellular carcinoma , cancer research , gene knockdown , tumor progression , downregulation and upregulation , medicine , metastasis , chemistry , cell culture , biology , renal function , cancer , gene , biochemistry , genetics
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.