Matrine suppresses breast cancer cell proliferation and invasion via VEGF-Akt-NF-κB signaling

Yu, Pengfei; Liu, Qian; K, Liu; Yagasaki, Kazumi; Wu, Erxi; Zhang, Guoying

doi:10.1007/s10616-009-9225-9

Cited by 109 publications

(110 citation statements)

References 21 publications

Supporting

Mentioning

103

Contrasting

Order By: Relevance

“…Activation of p-Akt and the NF-jB/Bcl-2 pathway leads to inhibition of chemotherapy-induced apoptosis, which results in treatment resistance (Wang et al 1996). Our previous results confirmed that suppression of Akt and the NF-jB/Bcl-2 pathway by anticancer agents inhibited growth and induced apoptosis and cell cycle arrest in A549 cells and breast cancer MDA-MB-231 cells (Wang et al 2009;Yu et al 2009). In the present study, we indicated that bufalin and the inhibitor of PI3 K/Akt (LY294002) and of NF-jB (Bay) inhibited the A549 cell proliferation and the PI3 K/Akt and NF-jB pathway by suppressing the phosphorylation and expressions of Akt and NF-jB and activating the apoptotic pathway of Bcl-2/Bax-mitochondrial-caspase-3 in A549 cells.…”

Section: Bufalin Reduces the Receptor Phosphorylation And/or Protein supporting

confidence: 69%

“…Flow cytometry for cell cycle analysis and apoptosis These were done according to our published methods (Wang et al 2009;Yu et al 2009;Zhang et al 2000). In brief, A549 cells were treated for 48 h with bufalin at concentrations of 0, 2.5, 5, and 10 lM.…”

Section: Cell Culture and In Vitro Proliferation Assaymentioning

confidence: 99%

“…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).…”

Section: Western Blot Analysismentioning

confidence: 99%

See 2 more Smart Citations

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

et al. 2010

Self Cite

View full text Add to dashboard Cite

Bufalin, a naturally occurring small-molecule compound from Traditional Chinese Medicine (TCM) Chansu showed inhibitory effects against human prostate, hepatocellular, endometrial and ovarian cancer cells, and leukemia cells. However, whether or not bufalin has inhibitory activity against the proliferation of human non-small cell lung cancer (NSCLC) cells is unclear. The aim of this study is to study the effects of bufalin on the proliferation of NSCLC and its molecular mechanisms of action. The cancer cell proliferation was measured by MTT assay. The apoptosis and cell cycle distribution were analyzed by flow cytometry. The protein expressions and phosphorylation in the cancer cells were detected by Western blot analysis. In the present study, we have demonstrated that bufalin suppressed the proliferation of human NSCLC A549 cell line in time-and dosedependent manners. Bufalin induced the apoptosis and cell cycle arrest by affecting the protein expressions of Bcl-2/Bax, cytochrome c, caspase-3, PARP, p53, p21WAF1, cyclinD1, and COX-2 in A549 cells. In addition, bufalin reduced the protein levels of receptor expressions and/or phosphorylation of VEGFR1, VEGFR2, EGFR and/or c-Met in A549 cells. Furthermore, bufalin inhibited the protein expressions and phosphorylation of Akt, NF-jB, p44/42 MAPK (ERK1/2) and p38 MAPK in A549 cells. Our results suggest that bufalin inhibits the human lung cancer cell proliferation via VEGFR1/VEGFR2/EGFR/cMet-Akt/p44/42/p38-NF-jB signaling pathways; bufalin may have a wide therapeutic and/or adjuvant therapeutic application in the treatment of human NSCLC.

show abstract

Section: Bufalin Reduces the Receptor Phosphorylation And/or Protein supporting

confidence: 69%

Section: Cell Culture and In Vitro Proliferation Assaymentioning

confidence: 99%

See 1 more Smart Citation

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

et al. 2010

Self Cite

View full text Add to dashboard Cite

show abstract

“…Flow cytometry for cell cycle analysis and apoptosis These were done according to our published methods (Wang et al 2009;Yu et al 2009;Zhang et al 2000Zhang et al , 2012a. In brief, LLC cells were treated for 48 h with sodium valproate (VPA, 0.5 mM), coumarin-3-carboxylic acid (HCCA, 0.064 mM), or in combination of VPA (0.5 mM) and HCCA (0.064 mM).…”

Section: Cell Culture and In Vitro Proliferation Assaymentioning

confidence: 99%

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

et al. 2012

Self Cite

View full text Add to dashboard Cite

Valproic acid (VPA) as a broad-spectrum inhibitor of histone deacetylase, has been used in cancer therapy. Recently, the combination of VPA with other anticancer agents has been considered as a useful and necessary strategy to inhibit tumor growth and progression. The coumarin derivates from natural plants have been shown to be the promising natural anticancer agents. However, no literature is available on the anticancer effects of the combination of VPA and coumarin-3-carboxylic acid (HCCA). Here we show that this combination significantly increases inhibitory effects against the proliferation and migration in highly-metastatic lung cancer cells by inducing apoptosis and cell cycle arrest as well as regulating related protein expressions. Our results indicate that this combination of VPA with HCCA not only enhances the protein levels of Bax, cytosolic cytochrome c, caspase-3 and PARP-1 but also reduces the protein expressions of Bcl-2, cyclin D1 and NF-jB as well as inhibits the phosphorylation and expressions of Akt, EGFR, VEGFR2 and c-Met in the cancer cells. Our results suggest that the combination of VPA with HCCA suppresses the proliferation and migration of lung cancer cells via EGFR/VEGFR2/c-Met-Akt-NFjB signaling pathways; this combination may have a wide therapeutic and/or adjuvant therapeutic application in the treatment of lung cancer.

show abstract

“…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.…”

Section: Introductionmentioning

confidence: 99%

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

Zhang

Shi

et al. 2013

Acta Pharmacol Sin

View full text Add to dashboard Cite

Aim: Vasodilator-stimulated phosphoprotein (VASP) expression is upregulated in human cancers and correlates with more invasive advanced tumor stages. The aim of this study was to elucidate the mechanisms by which matrine, an alkaloid derived from Sophora species plants, acted on the VASP protein in human gastric cancer cells in vitro. Methods: VASP was expressed and purified. Intrinsic fluorescence spectroscopy was used to study the binding of matrine to VASP. CD spectroscopy was used to examine the changes in the VASP protein secondary structure. Human gastric carcinoma cell line BGC823 was tested. Scratch wound and cell adhesion assays were used to detect the cell migration and adhesion, respectively. Real-time PCR and Western blotting assays were used to measure mRNA and protein expression of VASP. Results: In the fluorescence assay, the dissociation constant for binding of matrine to VASP protein was 0.86 mmol/L, thus the direct binding between the two molecules was weak. However, matrine (50 μg/mL) caused obvious change in the secondary structure of VASP protein shown in CD spectrum. Treatments of BGC823 cells with matrine (50 μg/mL) significantly inhibited the cell migration and adhesion. The alkaloid changed the subcellular distribution of VASP and formation of actin stress fibers in BGC823 cells. The alkaloid caused small but statistically significant decreases in VASP protein expression and phosphorylation, but had no significant effect on VASP mRNA expression. Conclusion: Matrine modulates the structure, subcellular distribution, expression and phosphorylation of VASP in human gastric cancer cells, thus inhibiting the cancer cell adhesion and migration.

show abstract

Matrine suppresses breast cancer cell proliferation and invasion via VEGF-Akt-NF-κB signaling

Cited by 109 publications

References 21 publications

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

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

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

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

Contact Info

Product

Resources

About