In vitro study of Bostrycin as a molecule target drug in lung cancer

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Author:
GUO Yu-biao(The First Affiliated Hospital, Sun Yat-sen University)
CHEN Wei-sheng(The First Affiliated Hospital, Sun Yat-sen University)
YANG Hui-ling()
LIN Yong-cheng()
SHE Zhi-gang()
Journal Title:
CHINESE JOURNAL OF BIOMEDICAL ENGINEERING
Issue:
Volume 15, Issue 06, 2009
DOI:
10.3760/cma.j.issn.1674-1927.2009.06.003
Key Word:
Lung cancer; Pharmacological mechanisms of action; Antineoplastic agents;Phosphatidylinositol 3 kinase/protein kinase B; A549 cells

Abstract: Objective To investigate the effect of the new-structure compound Bostrycin from marine fungi on the proliferation and apeptosis of lung cancer cell A549 in vitro, and to explore its mechanism.Methods A549 cells were complete randomly divided into treatment group and control group.A549 cells in treatment group were treated with different concentrations of Bostrycin for different time while cells in control group were not.The rate of proliferation of A549 cells before and after treatment was assessed with MTT method.Electron microscopy and flow cytometry were used to detect apoptosis of the cells.Real time PCR and Western blot were employed to explore the mechanism of Bostrycin.Results Bostrycin at a level of ≥ 10 μmol/L had a significant inhibitory effect on the proliferation of A549 ceil, and the 24-, 48-and 72-hour IC_(50) (inhibitory concentration of half) were 20.20, 14.36 and 9.42 μmol/L, respectively.Following Bostrycin interference, typical apoptotie appearance of A549 cells could be observed under electron microscope.Percentage increased for the cells at G_0/G_1 phase and decreased for the cells at S phase or G_2/M phase with increased apoptotic rate as were revealed by flow cytometry.Signal up-regulation was detected with real time RT-PCR in both micro RNA-638 and micro RNA-923, and decreased expression of the proteins p110 α and p- Akt and increased expression of p27 protein were found by Western blot.Conclusions Bostryein has significant inhibition on A549 cell proliferation possibly through suppression of PI3K/Akt pathway by micro RNAs.

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