BML-111, the analogue of lipoxin, inhibits Hela cell proliferation
10.3969/j.issn.1006-5725.2014.13.009
- VernacularTitle:脂氧素类似物BML-111抑制Hela细胞增殖及机制初探
- Author:
Hua HAO
;
Fen XU
;
Liqing WU
;
Xinxin ZHANG
;
Hua DAI
- Publication Type:Journal Article
- Keywords:
Uterine cervical neoplasms;
Lipoxin;
BML-111;
NF-κB
- From:
The Journal of Practical Medicine
2014;(13):2045-2047
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of BML-111 (the analogue of lipoxin) on uterine Hela cell (cervix cancer cell line) proliferation and the underlying mechanism. Methods Hela cells were stimulated by 50, 100, 200 and 400 μg/L BML-111, respectively, and cell viability was determined by MTT assay. Hela cells were divided into three groups:the control group (no treatment), the BML-111(200μg/L) group and the BML-111(200μg/L)plus Boc-2 (10μmol/L)group. Expression and location of P53 protein were detected by immunofluorescence. Expressions of NF-κB p65,P53 and CyclinD1 protein were detected by Western blotting. Results BML-111 (100, 200 and 400 μg/L) could effectively inhibit Hela cell viability compared with the control group (P < 0.05). P53 expression was shown decreased in both the nucleus and the cytoplasm without any change of P53 location , however, Boc-2 could reverse this effect. BML-111 could effectively inhibit P53 and CyclinD1 expression via NF-κB pathway and the effects could also be inhibited by Boc-2. Conclusions BML-111 can effectively inhibit Hela cell proliferation via FPR2 and NF-κB pathway.
