Antitumor effect of a pyrazolone-based-complex [Cu(PMPP-SAL)(EtOH)] against murine melanoma B16 cell in vitro and in vivo

AbstractPyrazolone-based derivative metal complexes were reported to have cytotoxicity in some tumor cells. In this study, the antitumor effect of [Cu(PMPP-SAL)(EtOH)] (PMPP-SAL = N-(1-phenyl-3-methyl-4-propenylidene-5-pyrazolone)- salicylidene hydrazide anion) in murine melanoma B16 cells in vitro and in vivo was investigated. The results showed that [Cu(PMPP-SAL)(EtOH)] inhibited the survival of B16 cells in vitro, and the IC50 value was superior to cisplatin (DDP) (p < 0.001). B16 cell apoptosis was significantly higher in comparison to the control group (DMSO) (p < 0.01), and cell cycle arrest occurred at the G0/G1 phase. When challenged C57 BL/6J mice were treated with [Cu(PMPPSAL)(EtOH)], a smaller volume of B16 solid tumors were reported than the control group (p < 0.01), with lower positive expression indices of CD 34, vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) (p < 0.01). Moreover, the tumor growth was suppressed in mice due to the induction of apoptosis, as detected by the TUNEL assay (p < 0.001). In summary, [Cu(PMPP-SAL)(EtOH)] effectively inhibited the growth of B16 cells in vitro and in vivo due to the induction of apoptosis and the inhibition of intra-tumoral angiogenesis, demonstrating its therapeutic potential in melanoma treatment.

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Evaluation of vascular endothelial growth factor and nitric oxide associated with resveratrol supplementation

European Journal of Public Health ◽

10.1093/eurpub/ckab120.108 ◽

2021 ◽

Vol 31 (Supplement_2) ◽

Author(s):

Armando Caseiro ◽

Carla Ferreira ◽

Ana Margarida Silva ◽

João Paulo Figueiredo ◽

Telmo Pereira

Keyword(s):

Nitric Oxide ◽

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Intervention Group ◽

Study Groups ◽

Control Group ◽

Vascular Endothelial ◽

Endothelial Growth Factor

Abstract Background Resveratrol (3,4',5-trihydroxystilbene) (RSV) is one of the main non-flavonoid natural polyphenol compounds. Evidence suggests that RSV has a key role in preventing a variety of pathological processes because of its benefits, including anti-aging, anti-inflammatory, and cardiovascular disease prevention. Vascular endothelial growth factor (VEGF) is responsible for vasculogenesis and angiogenesis, and its expression is influenced by RSV. Vascular nitric oxide (NO) acts to relax smooth muscle cells by preventing thrombogenic processes. It has been shown in vitro and in vivo that RSV is involved in NO metabolism. The aim of this work was evaluate the effects of regular low-dose RSV consumption by determining serum VEGF and NO levels compared to a control group. Methods The study involved 27 clinically healthy individuals, divided into a control group (placebo) and an intervention group, supplemented with 100mg RSV/day. The VEGF levels were determined by slot blot technique and NO levels were determined by spectrophotometry before (T0) and after 30 days (T1) of supplementation. Results The VEGF and NO levels slightly decrease from T0 to T1 moment in both study groups, showing a higher decrease in both parameters in the control group compared to the intervention group, but the variation was not statistically significant. Conclusions Daily supplementation with RSV is associated with benefits at the VEGF level as well as at the vascular level. However, further studies with a larger number of participants are needed to confirm the effects of RSV on VEGF and NO levels.

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Activation of β2-Adrenergic Receptor Promotes Growth and Angiogenesis in Breast Cancer by Down-regulating PPARγ

Cancer Research and Treatment ◽

10.4143/crt.2019.510 ◽

2020 ◽

Vol 52 (3) ◽

pp. 830-847 ◽

Cited By ~ 2

Author(s):

Jing Zhou ◽

Zhanzhao Liu ◽

Lingjing Zhang ◽

Xiao Hu ◽

Zhihua Wang ◽

...

Keyword(s):

Breast Cancer ◽

Growth Factor ◽

Chronic Stress ◽

Adrenergic Receptor ◽

Clinical Medicine ◽

Therapeutic Potential ◽

Control Group ◽

Pparγ Agonist

PurposeChronic stress and related hormones are key in cancer progression. Peroxisome proliferator-activated receptor γ (PPARγ) and its agonists was reported that inducing anti-tumor effect. However, the function of PPARγ in pro-tumorigenic effects induced by chronic stress in breast cancer remains unknown. Herein, we have characterized a novel role of PPARγ and vascular endothelial growth factor (VEGF)/fibroblast growth factor 2 (FGF2) signals in breast cancer promoted by chronic stress.Materials and MethodsWe performed experiments in vivo and in vitro and used bioinformatics data to evaluate the therapeutic potential of PPARγ in breast cancer promoted by stress.ResultsChronic stress significantly inhibited the PPARγ expression and promoted breast cancer in vivo. VEGF/FGF2-mediated angiogenesis increased in the chronic stress group compared to the control group. PPARγ agonist pioglitazone (PioG) injection offset the pro-tumorigenic effect of chronic stress. Moreover, specific β2-adrenergic receptor (β2R) antagonist ICI11-8551 inhibited the effect of chronic stress. In vitro, norepinephrine (NE) treatment had a similar tendency to chronic stress. The effect of NE was mediated by the β2R/adenylate cyclase signaling pathway and suppressed by PioG. PPARγ suppressed VEGF/FGF2 through reactive oxygen species inhibition. Bioinformatics data confirmed that therewas a lowPPARγ expression in breast invasive carcinoma. Lower PPARγ was associated with a significantly worse survival.Conclusion β2R activation induced by chronic stress and related hormones promotes growth and VEGF/FGF2-mediated angiogenesis of breast cancer by down-regulating PPARγ. Our findings hint that β receptor and PPARγ as two target molecules and the novel role for their agonists or antagonists as clinical medicine in breast cancer therapy

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Regulation of vascular endothelial growth factor expression in human endometrium by steroids and hypoxia: In vitro and in vivo studies

Journal of the Society for Gynecologic Investigation ◽

10.1016/s1071-5576(97)86195-3 ◽

1998 ◽

Vol 5 (1) ◽

pp. 69A-69A

Author(s):

A SHARKEY ◽

D CHARNOCKJONES ◽

K DAY ◽

H SOWTER ◽

L SVENSSON ◽

...

Keyword(s):

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Human Endometrium ◽

In Vivo Studies ◽

Vascular Endothelial ◽

Factor Expression ◽

Growth Factor Expression ◽

Endothelial Growth Factor

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Transgenic Overexpression of Vascular Endothelial Growth Factor-B Isoforms by Endothelial Cells Potentiates Postnatal Vessel Growth In Vivo and In Vitro

Circulation Research ◽

10.1161/01.res.0000182631.33638.77 ◽

2005 ◽

Vol 97 (6) ◽

Cited By ~ 38

Author(s):

Arne W. Mould ◽

Sonia A. Greco ◽

Marian M. Cahill ◽

Ian D. Tonks ◽

Daniela Bellomo ◽

...

Keyword(s):

Vascular Endothelial Growth Factor ◽

Endothelial Cells ◽

Growth Factor ◽

Vascular Endothelial ◽

Factor B ◽

Vessel Growth ◽

Endothelial Growth Factor

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Regulation of Vascular Endothelial Growth Factor by Tamoxifen in vitro and in vivo

Gynecologic and Obstetric Investigation ◽

10.1159/000070190 ◽

2003 ◽

Vol 55 (2) ◽

pp. 119-124 ◽

Cited By ~ 3

Author(s):

Michael D. Mueller ◽

Elizabeth A. Pritts ◽

Charles J. Zaloudek ◽

Ekkehard Dreher ◽

Robert N. Taylor

Keyword(s):

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Vascular Endothelial ◽

Endothelial Growth Factor

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Total saponins from Albizia julibrissin inhibit vascular endothelial growth factor-mediated angiogenesis in vitro and in vivo

Molecular Medicine Reports ◽

10.3892/mmr.2015.3228 ◽

2015 ◽

Vol 11 (5) ◽

pp. 3405-3413 ◽

Cited By ~ 9

Author(s):

WEIWEI CAI ◽

YUE LI ◽

QINGQING YI ◽

FENGSHAN XIE ◽

BIN DU ◽

...

Keyword(s):

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Vascular Endothelial ◽

Albizia Julibrissin ◽

Endothelial Growth Factor

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Vascular Endothelial Growth Factor Inhibits the Development of Dendritic Cells and Dramatically Affects the Differentiation of Multiple Hematopoietic Lineages In Vivo

Blood ◽

10.1182/blood.v92.11.4150 ◽

1998 ◽

Vol 92 (11) ◽

pp. 4150-4166 ◽

Cited By ~ 624

Author(s):

Dmitry Gabrilovich ◽

Tadao Ishida ◽

Tsunehiro Oyama ◽

Sophia Ran ◽

Vladimir Kravtsov ◽

...

Keyword(s):

Stem Cells ◽

Vascular Endothelial Growth Factor ◽

Dendritic Cells ◽

Growth Factor ◽

System Control ◽

Vascular Endothelial ◽

Almost All ◽

Endothelial Growth Factor

Abstract Defective function of dendritic cells (DC) in cancer has been recently described and may represent one of the mechanisms of tumor evasion from immune system control. We have previously shown in vitro that vascular endothelial growth factor (VEGF), produced by almost all tumors, is one of the tumor-derived factors responsible for the defective function of these cells. In this study, we investigated whether in vivo infusion of recombinant VEGF could reproduce the observed DC dysfunction. Continuous VEGF infusion, at rates as low as 50 ng/h (resulting in serum VEGF concentrations of 120 to 160 pg/mL), resulted in a dramatic inhibition of dendritic cell development, associated with an increase in the production of B cells and immature Gr-1+ myeloid cells. Infusion of VEGF was associated with inhibition of the activity of the transcription factor NF-κB in bone marrow progenitor cells. Experiments in vitro showed that VEGF itself, and not factors released by VEGF-activated endothelial cells, affected polypotent stem cells resulting in the observed abnormal hematopoiesis. These data suggest that VEGF, at pathologically relevant concentrations in vivo, may exert effects on pluripotent stem cells that result in blocked DC development as well as affect many other hematopoietic lineages.

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