Antiproliferative effect of β-escin - an in vitro study.

Mojžišová, Gabriela; Kello, Martin; Pilátová, Martina; Tomečková, Vladimı́ra; Vašková, Janka; Vaško, Ladislav; Bernatova, S; Mirossay, Ladislav; Mojžiš, Ján

doi:10.18388/abp.2015_1013

Cited by 21 publications

(11 citation statements)

References 55 publications

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“… 7 Recently, accumulated experimental evidence has shown that escin is a potential cancer chemotherapeutic and has elucidated some of the underlying mechanisms. 8 , 9 , 10 However, the principal mechanism underlying its anti-tumour effect is not fully understood. Furthermore, the effects of escin effect on human osteosarcoma and its underlying mechanisms have not been reported.…”

mentioning

confidence: 99%

Escin induces caspase-dependent apoptosis and autophagy through the ROS/p38 MAPK signalling pathway in human osteosarcoma cells in vitro and in vivo

Zhu

Liu

et al. 2017

Cell Death Dis

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Osteosarcoma is one of the most malignant neoplasms in adolescents, and it generally develops multidrug resistance. Escin, a natural mixture of triterpene saponins isolated from Aesculus hippocastanum (horse chestnut), has demonstrated potent anti-tumour potential in vitro and in vivo. In the present study, we found that escin inhibited osteosarcoma proliferation in a dose- and time-dependent manner. Additionally, escin-induced apoptosis was evidenced by the increased expression of caspase-related proteins and the formation of apoptotic bodies. Escin also induced autophagy, with elevated LC3, ATG5, ATG12 and Beclin expression as well as autophagosome formation. Inhibition of escin-induced autophagy promoted apoptosis. Moreover, p38 mitogen-activated protein kinases (MAPKs) and reactive oxygen species (ROS) were activated by escin. A p38 MAPK inhibitor partially attenuated the autophagy and apoptosis triggered by escin, but a ROS scavenger showed a greater inhibitory effect. Finally, the therapeutic efficacy of escin against osteosarcoma was demonstrated in an orthotopic model. Overall, escin counteracted osteosarcoma by inducing autophagy and apoptosis via the activation of the ROS/p38 MAPK signalling pathway; these findings provide evidence for escin as a novel and potent therapeutic for the treatment of osteosarcoma.

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confidence: 99%

Escin induces caspase-dependent apoptosis and autophagy through the ROS/p38 MAPK signalling pathway in human osteosarcoma cells in vitro and in vivo

Zhu

Liu

et al. 2017

Cell Death Dis

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“…β-Escin treatment at the concentration of 60 μg/mL did not increased sub-G1 population (apoptotic cells) likely making this plant-based compound suitable for further experiments. More importantly, our extract was previously tested on selected cancer cell lines [ 19 ] where we clearly demonstrated anti-proliferative concentrations in the IC 50 ranged from 21.2 µg/mL to 42.9 µg/mL. Hence, we found different sensitivity of cancer and non-cancer cells which might be of clinical importance.…”

Section: Discussionmentioning

confidence: 75%

“…Several studies reported that β-escin and its derivatives are also prime candidates as potential cancer chemotherapeutic agents [ 18 , 19 , 20 , 21 ]. Recent studies have shown that β-escin has anti-proliferative effects in different cancer cell lines.…”

Section: Introductionmentioning

confidence: 99%

β-Escin Effectively Modulates HUVECs Proliferation and Tube Formation

et al. 2018

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In the present study we evaluated the anti-angiogenic activities of β-escin (the major active compound of Aesculus hippocastanum L. seeds). Human umbilical-vein endothelial cells (HUVECs) were used as an in vitro model for studying the molecular mechanism underlying the anti-angiogenic effect of β-escin. We investigated the in vitro effects on proliferation, migration, and tube formation of HUVECs and in vivo anti-angiogenic activity was evaluated in a chick chorioallantoic membrane (CAM) angiogenesis assay. Moreover, the effect on gene expressions was determined by the RT2 ProfilerTM human angiogenesis PCR Array. It was found that β-escin exerts inhibitory effect on the basic fibroblast growth factor (bFGF)-induced proliferation, migration and tube formation, as well as CAM angiogenesis in vivo. The inhibition of critical steps of angiogenic process observed with β-escin could be partially explained by suppression of Akt activation in response to bFGF. Moreover, the anti-angiogenic effects of β-escin could also be mediated via inhibition of EFNB2 and FGF-1 gene expressions in endothelial cells. In conclusion, β-escin affects endothelial cells as a negative mediator of angiogenesis in vitro and in vivo and may therefore be considered as a promising candidate for further research elucidating its underlying mechanism of action.

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“…Colonies were fixed with 70% ethanol and stained with 0.5% crystal violet. [2021] In the next step, the image of the colonies was taken, and plating efficiency (PE) was measured using the following formula; (number of colonies/number of seeded cells) × 100 and surviving fraction (SF) was determined by (number of colonies/number of seeded cells × PE control) × 100. [22]…”

Section: Methodsmentioning

confidence: 99%

Activation of p53 gene expression and synergistic antiproliferative effects of 5-fluorouracil and β-escin on MCF7 cells

Mazrouei

Raeisi

Lemoigne³

et al. 2019

J Med Signals Sens

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One of the most common malignancies in women is breast cancer. β-escin has pharmacological anticancer effects. 5-fluorouracil (5-FU) has antimetabolite and antiproliferative properties. The purpose of this study was to investigate the combined effects of 5-FU and β-escin on apoptosis, colony formation, Bcl-2 signaling protein, and p53 gene expression in MCF7 breast cancer cell line. The cytotoxic effects, the number of colonies, apoptosis, p53 gene expression, and Bcl-2 signaling protein of the combined 5-FU and β-escin on MCF7 cells were determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, clonogenic assay, flow cytometry, real-time quantitative polymerase chain reaction, and western blotting methods, respectively. Half-maximal inhibitory concentration values of β-escin and 5-FU were 80 μg/ml and 2 μM, respectively. The combination of 5-FU and β-escin on MCF7 cell viability showed a combination index equal to 0.5. The expression of p53 and apoptosis increased in the combination of 5-FU and β-escin on MCF7 cells compared to that of control group (P < 0.05). In addition, the number of colonies and Bcl-2 signaling protein in combination of 5-FU and β-escin decreased with respect to untreated control cells or single treatment of 5-FU and β-escin. The combination of 5-FU and β-escin not only has synergistic effects by increasing cell apoptosis and p53 gene expression but also decreases Bcl-2 signaling protein in MCF7 cell lines.

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Antiproliferative effect of β-escin - an in vitro study.

Cited by 21 publications

References 55 publications

Escin induces caspase-dependent apoptosis and autophagy through the ROS/p38 MAPK signalling pathway in human osteosarcoma cells in vitro and in vivo

Escin induces caspase-dependent apoptosis and autophagy through the ROS/p38 MAPK signalling pathway in human osteosarcoma cells in vitro and in vivo

β-Escin Effectively Modulates HUVECs Proliferation and Tube Formation

Activation of p53 gene expression and synergistic antiproliferative effects of 5-fluorouracil and β-escin on MCF7 cells

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