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Inhibition of cytosolic chaperonin CCTζ‐1 expression depletes proliferation of colorectal carcinoma in vitro
Author(s) -
QianLin Zhu,
TingFeng Wang,
QiFeng Cao,
MinHua Zheng,
AiGuo Lu
Publication year - 2010
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.21625
Subject(s) - western blot , apoptosis , cell growth , colorectal cancer , cancer research , medicine , immunohistochemistry , transfection , carcinogenesis , annexin , microbiology and biotechnology , gene silencing , pathology , cancer , cell culture , biology , staining , gene , biochemistry , genetics
Background It is important to identify the behavior of colorectal cancer (CRC) individually, so more accurate laboratory index is urgently demanded. Chaperonin are key molecules in tumor cell cycle. Our study aims at revealing the expression and correlation of chaperonin containing TCP1 complex 6A (CCTζ‐1) in CRC. Methods Fifty‐eight patients with CRC admitted from 2005 to 2008 were selected. CCTζ‐1 expression in cell, tumor, and non‐tumor colorectal tissues was detected by Western blot, and their protein was localized by immunohistochemical stain. After HCT116 cells were transfected with CCTζ‐1 siRNA, real‐time PCR, and Western blot were used to examine gene expression. Cell multiplication and apoptosis were examined by Cell Counting Kit‐8 and Annexin V kit. Results CCTζ‐1 ptotein expression was detected in 51 of 58 (87.9%) CRC specimens, which was much higher than those in normal mucosa ( P < 0.01), and it was correlated with tumor invasion ( P < 0.01) and tumor size ( P < 0.05). The levels of CCTζ‐1 mRNA and protein were inhibited by CCTζ‐1 siRNA in HCT116 cells transfected with CCTζ‐1 siRNA, which resulted in growth arrest but not apoptosis. Conclusion CCTζ‐1 could be a new prognostic marker for CRC and involve in tumorigenesis. CCTζ‐1 inhibition in vivo might therefore become a new therapy for CRC. J. Surg. Oncol. 2010;102:419–423. © 2010 Wiley‐Liss, Inc.