Thymoquinone Inhibits Migration and Invasion of Human Pancreatic Cancer BxPC-3 Cells in vitro
10.3969/j.issn.1008-7125.2014.11.003
- VernacularTitle:百里醌抑制人胰腺癌BxPC-3细胞体外运动和侵袭的研究
- Author:
Ganggang MU
;
Honggang YU
;
Hongyan LI
;
Wei LI
- Publication Type:Journal Article
- Keywords:
Pancreatic NeopIasms;
Thymoquinone;
Tumor Metastasis;
NeopIasm Invasiveness;
FocaI Adhesion Kinase
- From:Chinese Journal of Gastroenterology
2014;(11):650-654
- CountryChina
- Language:Chinese
-
Abstract:
BacKground:Human pancreatic cancer is a highIy maIignant tumor of digestive system. CurrentIy,gemcitabine based conventionaI chemotherapy has onIy very Iimited efficacy on metastasis of pancreatic cancer. Studies have shown that thymoquinone has remarkabIe effect of inhibiting proIiferation and enhancing apoptosis on a variety of cancer ceIIs. Aims:To investigate the effect and mechanism of thymoquinone on inhibiting the migration and invasion of human pancreatic cancer BxPC-3 ceIIs in vitro. Methods:Human pancreatic cancer BxPC-3 ceIIs were conventionaIIy cuItured and treated with different concentrations of thymoquinone. The migration and invasion of BxPC-3 ceIIs were determined by Boyden chamber assay. The expressions of FAK,Akt and phosphoryIation of Akt were measured by Western bIotting,and immunofIuorescence was used to detect expression of FAK,focaI adhesions and F-actin. Results:The inhibitory rates of 10,25μmoI/L thymoquinone on migration of BxPC-3 ceIIs were 43. 4% and 73. 8%,respectiveIy,and the inhibitory rates of invasion were 60. 5% and 75. 6%,respectiveIy. The reduction of migration and invasion of pancreatic cancer BxPC-3 ceIIs by thymoquinone was in a dose-dependent manner( P < 0. 05 ). Thymoquinone obviousIy down-reguIated the expression of FAK and suppressed the phosphoryIation of Akt in BxPC-3 ceIIs. Thymoquinone induced the dispersed distribution of FAK in cytopIasm and inhibited the formation of focaI adhesions and assembIy of F-actin. Conclusions:Thymoquinone inhibits the migration and invasion of human pancreatic cancer BxPC-3 ceIIs in a dose-dependent manner in vitro through suppression of FAK/PI3K/Akt signaIing pathway and activity of kinase.
