Apigenin Inhibits Expression of Vascular Endothelial Growth Factor and Angiogenesis in Human Lung Cancer Cells: Implication of Chemoprevention of Lung Cancer

@article{Liu2005ApigeninIE,
  title={Apigenin Inhibits Expression of Vascular Endothelial Growth Factor and Angiogenesis in Human Lung Cancer Cells: Implication of Chemoprevention of Lung Cancer},
  author={Ling-Zhi Liu and Jing Fang and Qiong Zhou and Xiaowen Hu and Xianglin Shi and Bing-Hua Jiang},
  journal={Molecular Pharmacology},
  year={2005},
  volume={68},
  pages={635 - 643}
}
Apigenin is a natural dietary flavonoid. It has recently been shown to have anticancer effects on prostate and ovarian cancer cells. However, the molecular basis of the effect of apigenin on cancer cells remains to be elucidated. In this study, we found that apigenin inhibited A549 lung cancer cell proliferation and vascular endothelial growth factor (VEGF) transcriptional activation in a dose-dependent manner. In an attempt to understand the mechanism of apigenin-inhibited VEGF expression, we… 
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The results identify apigenin as a bioflavonoid that inhibits hypoxia‐activated pathways linked to cancer progression in human prostate cancer, in particular the PI3K/Akt/GSK‐3 pathway.

Apigenin suppresses tumor angiogenesis and growth via inhibiting HIF-1α expression in non-small cell lung carcinoma.

Apigenin inhibited migration and invasion of human ovarian cancer A2780 cells through focal adhesion kinase.

It is demonstrated that apigenin inhibits expression of focal adhesion kinase (FAK) and migration and invasion of human ovarian cancer A2780 cells, and molecular targeting of FAK by Apigenin might be a useful strategy for chemoprevention and/or chemotherapeutics of ovarian cancers.

Inhibition of Cell Growth and VEGF Expression in Ovarian Cancer Cells by Flavonoids

Six flavonoids, including apigenin, taxifolin, luteolin, quercetin, genistein, and kaempferol, were shown to inhibit the ovarian cancer cell growth in a dose-dependent manner and naringin showed the least inhibition effect.

Apigenin down-regulates the hypoxia response genes: HIF-1α, GLUT-1, and VEGF in human pancreatic cancer cells.

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Kaempferol inhibits VEGF expression and in vitro angiogenesis through a novel ERK-NFκB-cMyc-p21 pathway.

Oral Administration of Apigenin Inhibits Metastasis through AKT/P70S6K1/MMP-9 Pathway in Orthotopic Ovarian Tumor Model

For the first time, oral uptake of apigenin can inhibit tumor metastasis through MMP-9 expression using the orthotopic ovarian tumor model and it is demonstrated that the downregulation of M MP-9 by apigen in was mediated by the AKT/p70S6K1 pathway.

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86 References

Signal pathways involved in apigenin inhibition of growth and induction of apoptosis of human anaplastic thyroid cancer cells (ARO).

Apigenin is a promising inhibitor of signal transduction pathways that regulate the growth (anchorage-dependent and independent) and survival of human anaplastic thyroid cancer cells.

9-β-d-Arabinofuranosyl-2-fluoroadenine Inhibits Expression of Vascular Endothelial Growth Factor through Hypoxia-Inducible Factor-1 in Human Ovarian Cancer Cells

A new function of Fara-A is demonstrated in inhibiting VEGF and HIF-1α expression and a potential molecular mechanism of the regulation is identified.

Apigenin inhibits growth and induces G2/M arrest by modulating cyclin-CDK regulators and ERK MAP kinase activation in breast carcinoma cells.

The results suggest that apigenin is a promising antibreast cancer agent and its growth inhibitory effects are mediated by targeting different signal transduction pathways in MCF-7 and MDA-MB-468 breast carcinoma cells.

Molecular mechanisms for apigenin‐induced cell‐cycle arrest and apoptosis of hormone refractory human prostate carcinoma DU145 cells

The molecular mechanism of inhibitory action of apigenin on androgen‐refractory human prostate carcinoma DU145 cells that have mutations in the tumor suppressor gene p53 and pRb was demonstrated to be modulation in cell‐cycle machinery, disruption of mitochondrial function, and NF‐κB inhibition.

Selective growth-inhibitory, cell-cycle deregulatory and apoptotic response of apigenin in normal versus human prostate carcinoma cells.

Apigenin may be developed as a promising chemopreventive and/or chemotherapeutic agent against prostate cancer and in a variety of prostate carcinoma cells representing different stage and androgen responsiveness.

Effects of deguelin on the phosphatidylinositol 3-kinase/Akt pathway and apoptosis in premalignant human bronchial epithelial cells.

The ability of deguelin to inhibit PI3K/Akt-mediated signaling pathways may contribute to the potency and specificity of this pro-apoptotic drug.

Arsenite induces HIF-1α and VEGF through PI3K, Akt and reactive oxygen species in DU145 human prostate carcinoma cells

It is demonstrated that arsenite induces the expression of Hif-1α but not HIF-1β subunit in DU145 human prostate carcinoma cells, indicating that the arsenite-induced activation of PI3K/Akt signaling and theexpression of H IF-1 and VEGF through the generation of ROS could be an important mechanism in the arsenITE-induced carcinogenesis.

Flavonoids inhibit VEGF/bFGF‐induced angiogenesis in vitro by inhibiting the matrix‐degrading proteases

The data suggest that genistein, apigenin, and 3‐hydroxyflavone inhibit in vitro angiogenesis, in part via preventing VEGF/bFGF‐induced MMP‐1 and uPA expression and the activation of pro‐MMP‐2, and via modulating their inhibitors, TIMP‐1and ‐2 and PAI‐1.

Insulin-like Growth Factor 1 Induces Hypoxia-inducible Factor 1-mediated Vascular Endothelial Growth Factor Expression, Which is Dependent on MAP Kinase and Phosphatidylinositol 3-Kinase Signaling in Colon Cancer Cells*

It is demonstrated that exposure of HCT116 human colon carcinoma cells to IGF-1 induces the expression of HIF-1α, the regulated subunit of hypoxia-inducible factor 1, a known transactivator of the VEGF gene.

Squamous Cell Carcinoma Related Oncogene Regulates Angiogenesis through Vascular Endothelial Growth Factor-A

VEGF-A expression correlates with SCCRO expression in these primary human lung squamous cell carcinomas and is a predictor of clinical behavior, which supports the association of SCRRO and VEGF-A in the induction of angiogenesis.
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