Wentilactone A inhibition of migration of small cell lung carcinoma NCI-H1688 cell line
10.3969/j.issn.1006-0111.2016.03.007
- VernacularTitle:Wentilactone A抑制小细胞肺癌系NCI-H1688细胞的迁移研究
- Author:
Wenli JIANG
1
;
Caiguo HUANG
Author Information
1. 第二军医大学基础部生物化学与分子生物学教研室
- Keywords:
Wentilactone A;
SCLC;
migration;
proliferation
- From:
Journal of Pharmaceutical Practice
2016;34(3):219-222,274
- CountryChina
- Language:Chinese
-
Abstract:
Objective ToinvestigatemechanismofWentilactoneA (WA)inhibitionofsmallcelllungcancer(SCLC)cell line NCI-H1688 migration .Methods The migration and proliferation were analyzed by wounding-healing assay and MTT assay [3-(4 ,5-Dimethylthiazol-2-yl)-2 ,5-diphenyltetrazolium bromide ,MTT] .Immunofluorescence was used to confirm the ex-pression of ATF3 protein after WA treatment .Western blot was used to examine the expression of key proteins in ATF3/Nrf2/AKR1C1 signal pathway .Results WA inhibits the proliferation and migration of SCLC .MTT analysis showed WA in-hibits the proliferation of NCI-H1688 cell line in a time-dependent manner .The number of migrated cells in WA treatment group was (8 .73 ± 1 .06) mm ,which was lower than that of control group (15 .63 ± 3 .11) mm ,The number of migrated cells in AKR1C1 expression group was (24 .37 ± 0 .90) mm ,the number of migrated cells in AKR1C1 expression and WA treatment group was (14 .17 ± 1 .31) mm ,with significant difference (P<0 .05) .WA enhances the nuclear expression of ATF3 ,and then reduces the expression of p-Nrf2 and AKR1C1 .Conclusion WA inhibits the proliferation and migration of SCLC through ATF3/Nrf2/AKR1C1 signal pathway .
