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Chaperonin containing TCP 1, subunit 8 ( CCT 8) is upregulated in hepatocellular carcinoma and promotes HCC proliferation
Author(s) -
Huang Xiaodong,
Wang Xingxiu,
Cheng Chun,
Cai Jing,
He Song,
Wang Hua,
Liu Fang,
Zhu Changlai,
Ding Zongmei,
Huang Xianting,
Zhang Tianyi,
Zhang Yixin
Publication year - 2014
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12258
Subject(s) - hepatocellular carcinoma , western blot , immunohistochemistry , oncogene , cell growth , cancer research , biology , pathogenesis , downregulation and upregulation , chaperonin , cell cycle , cell , pathology , microbiology and biotechnology , immunology , medicine , protein folding , gene , biochemistry , genetics
The development of molecular pathogenesis of hepatocellular carcinoma ( HCC ) is complex and involves alterations in the expression and conformation of assorted oncoproteins and tumor suppressors. Chaperonin containing TCP 1 ( CCT ) is a cytolic molecular chaperone complex that is required for the correct folding of numerous proteins. In this study, we investigated a possible involvement of CCT subunit 8 ( CCT 8) in HCC development. Immunohistochemical analysis was performed in 102 human HCC samples. High CCT 8 expression was detected in clinical HCC samples compared with adjacent noncancerous tissues. The univariate and multivariate survival analyses were also performed to determine their prognostic significance. Western blot confirmed the high expression of CCT 8 in HCC compared with adjacent normal tissue. Moreover, the biological significance of the aberrant expression of CCT 8 was investigated in HCC cell lines. Expression of CCT 8 was correlated directly with the histologic grades and tumor size of HCC and high expression of CCT 8 was associated with a poor prognosis. CCT 8 depletion by si RNA inhibited cell proliferation and blocked S‐phase entry in HuH7 cells. These results suggested that CCT 8 might be an oncogene and participate in HCC cell proliferation. These findings provide a potential therapeutic strategy for the treatment of HCC .