Inhibition of cytosolic chaperonin CCTζ-1 expression depletes proliferation of colorectal carcinoma in vitro
✍ Scribed by Zhu Qian-Lin; Wang Ting-Feng; Cao Qi-Feng; Zheng Min-Hua; Lu Ai-Guo
- Book ID
- 102441095
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 218 KB
- Volume
- 102
- Category
- Article
- ISSN
- 0022-4790
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
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.