Mechanism of polycomb Bmi1-targeted therapy for colorectal cancer.
- Author:
Hui ZHANG
1
;
Ying-jiang YE
;
Zhi-rong CUI
;
Shan WANG
Author Information
- Publication Type:Journal Article
- MeSH: Aged; Apoptosis; Cell Line, Tumor; Cell Proliferation; Colorectal Neoplasms; metabolism; pathology; Female; Humans; Male; Middle Aged; Neoplasm Staging; Polycomb Repressive Complex 1; metabolism; Proto-Oncogene Proteins c-bcl-2; metabolism
- From: Chinese Journal of Gastrointestinal Surgery 2011;14(8):623-626
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the Bmi1 protein level in human colorectal cancer specimen and associated clinicopathological parameters, and to determine the influence of Bmi1 on the proliferation and apoptosis of colorectal cancer cells.
METHODSBmi1 protein level was assessed in 85 patients with colorectal cancer and adjacent normal tissue by immunohistochemistry. SW480 cells were transfected with Bmi siRNA plasmid. MTT assay and flow cytometry were used to measure the proliferation and apoptosis of SW480 cells. The expression of Bmi1 and Bcl-2 were measured by Western blot.
RESULTSThe positive rate of Bmi1 expression in colorectal cancer tissues was 56.5%(48/85), significantly higher than that in the adjacent noncancerous tissues[17.6%(15/85), P<0.05)]. It was found that the overexpression of Bmi1 was associated with degree of differentiation, status of lymph nodes metastasis, and TNM staging in colorectal cancer(P<0.05). After transfection of SW480 with Bmi1 siRNA, the cell proliferation was inhibited and the apoptosis was significant. The cell proliferation inhibitory rates were 13.1%, 16.5%, and 18.3% at 24 h, 48 h and 72 h after transfection. The apoptotic rates were 15.7%, 45.6%, 40.2%, respectively. Expression of Bmi1 was downregulated after 48 h, as was that of Bcl-2.
CONCLUSIONSBmi1 expression is associated with the clinicopathological characteristics of colorectal cancer. Blockade of Bmi1 can inhibit the proliferation and accelerate the apoptosis of colorectal cancer cells.