Expression of secreted frizzled-related protein 4 in DNA mismatch repair-deficient and mismatch repair-proficient colorectal cancers.
10.12122/j.issn.1673-4254.2018.11.04
- Author:
Kexu CHEN
1
;
Hanlin LIANG
1
;
Jiewen PENG
1
;
Yanfang ZHENG
2
Author Information
1. Center of Oncology, Zhongshan People's Hospital, Zhongshan 528400, China.
2. Center of Oncology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.
- Publication Type:Journal Article
- Keywords:
apoptosis;
colorectal cancer;
mismatch repair;
proliferation;
secreted frizzled-related protein 4
- MeSH:
Apoptosis;
Cell Proliferation;
Colon;
metabolism;
pathology;
Colonic Neoplasms;
genetics;
metabolism;
pathology;
Colorectal Neoplasms;
genetics;
metabolism;
pathology;
DNA Mismatch Repair;
Gene Knockdown Techniques;
HCT116 Cells;
Humans;
Ki-67 Antigen;
metabolism;
Prognosis;
Proto-Oncogene Proteins;
genetics;
metabolism;
Up-Regulation
- From:
Journal of Southern Medical University
2018;38(11):1300-1305
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the expressions of secreted frizzled-related protein 4 (SFRP4) in stage Ⅱ DNA mismatch repair-deficient (dMMR) and mismatch repair- proficient (pMMR) colorectal cancers and explore their clinical significance.
METHODS:We collected fresh stage Ⅱ colon cancer tissues with different MMR status detected by immunohistochemistry (IHC). The differentially expressed mRNAs between dMMR and pMMR tumors were identified by Affymetrix Human oeLncRNA gene chip, and the expression of SFRP4 in these cancer tissues and in colorectal cancer cell lines were detected using Western blotting and real- time quantitative PCR. The apoptosis rates of HCT116 cells with and without siRNA- mediated transient SFRP4 knockdown were determined using flow cytometry. We further investigated the expression pattern of Ki-67 and its correlation with SFRP4 expression.
RESULTS:Compared with pMMR colon cancer tissues or cells, both dMMR colon cancer tissues (=0.014) and cells (=0.0079) showed significantly increased expression of SFRP4, which was in negative correlation with Ki-67 (=0.041). In HCT116 cells, transient SFRP4 knockdown resulted in decreased cell apoptosis, including both early apoptosis (=0.003) and late apoptosis (=0.024).
CONCLUSIONS:Up-regulation of SFRP4 in dMMR stage Ⅱ colon cancer promotes apoptosis and inhibits proliferation of the cancer cells, and may improve the prognosis of dMMR colon cancer.
