Effects of matrine against the growth of human lung cancer and hepatoma cells as well as lung cancer cell migration

Abstract

The purpose of this study is to investigate in vitro and ex vivo effects of matrine on the growth of human lung cancer and hepatoma cells and the cancer cell migration as well as the expressions of related proteins in the cancer cells. Matrine significantly inhibited the in vitro and ex vivo growth of human non-small cell lung cancer A549 and hepatoma SMMC-7721 cells. Matrine induced the apoptosis in A549 and SMMC-7721 cells. Western blot analysis indicated that matrine dose-dependently down-regulated the expression of anti-apoptotic protein Bcl-2 and up-regulated the level of pro-apoptotic protein bax, eventually leading the reduction of ratios of Bcl-2/Bax proteins in A549 and SMMC-7721 cells. Furthermore, matrine significantly suppressed the A549 cell migration without reducing the cell viability. In addition, matrine dramatically reduced the secretion of vascular endothelial growth factor A in A549 cells. More importantly, matrine markedly enhanced the anticancer activity of anticancer agent trichostatin A (the histone deacetylase inhibitor) by strongly reducing the viability and/or the ratio of Bcl-2/Bax protein in A549 cells. Our findings suggest that matrine may have the broad therapeutic and/or adjuvant therapeutic application in the treatment of human non-small cell lung cancer and hepatoma.

Matrine inhibits the adhesion and migration of BCG823 gastric cancer cells by affecting the structure and function of the vasodilator-stimulated phosphoprotein (VASP)

“…The phosphorylation of VASP at Ser157 was also significantly inhibited in BGC823 cells by treatment with 50 μg/mL of matrine, demonstrating that matrine could affect the structure and function of VASP through the inhibition of VASP phosphorylation in these cells. These findings agree with previous reports describing the effects of matrine on other types of cancer cells [6,8,18,28,29] . Ena/VASP proteins display a conserved tripartite architecture that encompasses an N-terminal Ena/VASP homology 1 (EVH1) domain that is required for subcellular targeting, a central proline-rich domain that is implicated in the recruitment of profilin-actin complexes, and a C-terminal EVH2 domain that mediates tetramerization and interaction with globular (G) and filament (F) actins [28,29] .…”

“…Matrine has been reported to inhibit human cancer cell migration, adhesion and proliferation by inhibiting the phosphorylation of VASP [6,8,[16][17][18] . However, the precise mechanism by which matrine acts directly on VASP remains unknown.…”

Enhanced suppression of proliferation and migration in highly-metastatic lung cancer cells by combination of valproic acid and coumarin-3-carboxylic acid and its molecular mechanisms of action

“…This was performed according to our published methods with some modifications (Wang et al 2009;Yu et al 2009;Zhang et al 2009Zhang et al , 2012aJiang et al 2010). In brief, LLC cells were treated with different concentrations of sodium valproate (VPA, 0.5-1 mM), coumarin-3-carboxylic acid (HCCA, 0.064-0.125 mM), or in combination of VPA and HCCA, or Ly294002 (Ly, 0.0125 mM), Bay (0.0025 mM).…”

Effects of bufalin on the proliferation of human lung cancer cells and its molecular mechanisms of action

“…This was performed according to our published methods with some modifications (Wang et al 2009;Yu et al 2009;Zhang et al 2009). In brief, A549 cells were treated with bufalin (0, 2.5, 5 and 10 lM), or Ly294002 (LY, 50 lM), Bay (10 lM), PD98059 (PD, 7 lM), and SB203580 (SB, 50 lM).…”