Effect of Juglone on Migration of Human Ovarian Cancer SKOV3 Cells

2014 ◽  
Vol 912-914 ◽  
pp. 1911-1914
Author(s):  
Liang Zhong Zhao ◽  
Shuang Chen ◽  
Qing Fang ◽  
Duo Zhang ◽  
You Peng Zhu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Wound Healing ◽  
Plant Species ◽  
Human Ovarian Cancer ◽  
Skov3 Cell ◽  
Potential Candidate ◽  
Wound Healing Assay ◽  
Skov3 Cells ◽  
Anti Cancer ◽  
Cancer Activity

Juglone is isolated from many plant species belonging to Juglandaceae family. Recent studies have shown that Juglone exhibits various bioactivities including anti-tumor functions. However, its anti-cancer activity on human ovarian cancer SKOV3 cell has not been examined. Thus, the current study was designed to elucidate the effect of Juglone on migration of human ovarian cancer SKOV3 cells. In the present study, SKOV3 cells were incubated with Juglone at various concentrations. Wound healing assay and Transwell chambers were used to detect migration of SKOV3 treated with Juglone for 24h. The result showed that Juglone inhibited the migration of SKOV3 cells with concentration of Juglone at 25, 50 or 100μM compared with control cells. Therefore, our results indicated that Juglone may be a potential candidate of drug for ovarian cancer.

scholarly journals S-Phase Cell Cycle Arrest, Apoptosis, and Molecular Mechanisms of Aplasia Ras homolog Member I–Induced Human Ovarian Cancer SKOV3 Cell Lines

2014 ◽  
Vol 24 (4) ◽  
pp. 629-634 ◽  
Author(s):  
Qiaoying Zhu ◽  
Jianming Hu ◽  
Huijuan Meng ◽  
Yufei Shen ◽  
Jinhua Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Molecular Mechanisms ◽  
Significant Inhibition ◽  
S Phase ◽  
Phase Cell ◽  
Cell Cycle Distribution ◽  
Human Ovarian Cancer ◽  
Skov3 Cell ◽  
Skov3 Cells

ObjectiveAplasia Ras homolog member I (ARHI) is associated with human ovarian cancer (HOC) growth and proliferation; however, the mechanisms are unclear. The purpose of this study was to investigateARHIeffects in HOC SKOV3 cells.MethodsWe transfected SKOV3 cells with PIRES2-EGFP-ARHI and measured growth inhibition rates, cell cycle distribution, apoptosis rates, and expression of P-STAT3 (phosphorylated signal transduction and activators of transcription 3) and P-ERK (phosphorylated extracellular signal regulated protein kinase).ResultsOur data showed significant inhibition of growth, significantly increased S-phase arrest and apoptosis rates, and reduction of P-STAT3 and P-ERK1/2 expression levels.ConclusionsWe propose the mechanism may involveARHI-induced phosphorylation of ERK1/2 and STAT3 protein kinases, thereby blocking proliferation signaling pathways, to induce HOC SKOV3 apoptosis.

A mechanistic study on the anti-cancer activity of ethyl caffeate in human ovarian cancer SKOV-3 cells

2014 ◽  
Vol 219 ◽  
pp. 151-158 ◽  
Author(s):  
Ha Neul Lee ◽  
Jin-Kyu Kim ◽  
Jae Hyeon Kim ◽  
Sang-Jin Lee ◽  
Eun-Kyung Ahn ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Mechanistic Study ◽  
Human Ovarian Cancer ◽  
Anti Cancer ◽  
Cancer Activity

scholarly journals Role of JNK Activation and Mitochondrial Bax Translocation in Allicin-Induced Apoptosis in Human Ovarian Cancer SKOV3 Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Ling Xu ◽  
Jin Yu ◽  
Dongxia Zhai ◽  
Danying Zhang ◽  
Wei Shen ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Cancer Cell Line ◽  
Biologically Active ◽  
Cell Counting ◽  
Human Ovarian Cancer ◽  
Skov3 Cell ◽  
Dependent Manner ◽  
Skov3 Cells ◽  
Induced Apoptosis ◽  
Jnk Activation

Background. Allicin, the major component of freshly crushed garlic, is one of the most biologically active compounds of garlic; it has been reported to induce apoptosis in cancer cells; however, the mechanism by which allicin exerts its apoptotic effects is not fully understood. The aim of the present study was to further elucidate the apoptotic pathways induced by allicin in the human ovarian cancer cell line SKOV3.Methods. Cell proliferation and apoptosis were measured by cell-counting assay and flow cytometry analysis. Activation of the signaling pathway was screened by human phospho-kinase array analysis, and the activated pathway and its related proteins were further confirmed by western blot analysis.Results. Allicin induced SKOV3 cell apoptosis and JNK phosphorylation in a time- and dose-dependent manner, but these were significantly blocked by SP600125 (an inhibitor of JNK). The findings suggest that JNK phosphorylation is related to the action of allicin on SKOV3 cells. Furthermore, JNK activation induced Bcl-2 family activation, triggered mitochondria-mediated signaling pathways, and led to the translocation of a considerable amount of Bax and cytochromecrelease.Conclusions. JNK activation and mitochondrial Bax translocation are involved in allicin-induced apoptosis in SKOV3 cells. Our data input new insights to the literature of allicin-induced apoptosis.

scholarly journals Sevoflurane inhibits the progression of ovarian cancer through down-regulating stanniocalcin 1 (STC1)

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Chuanfeng Zhang ◽  
Baosheng Wang ◽  
Xiuqin Wang ◽  
Xiugui Sheng ◽  
Yongchun Cui
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cancer Cell ◽  
Colony Formation ◽  
Ovarian Cancer Cell ◽  
Dependent Manner ◽  
Skov3 Cells ◽  
Anti Cancer ◽  
Cancer Activity

Abstract Background Ovarian cancer is one of the leading causes of female death worldwide, with a poor prognosis of advanced patients. Sevoflurane, a volatile anesthetic commonly used in clinical operations, has been reported to have anti-cancer activity against some tumors. In the present study, we aimed to investigate the effects of sevoflurane on the progression of ovarian cancer and its potential mechanism. Methods The effects of sevoflurane on ovarian cancer cell viability, proliferation, migration, invasion, cell cycle, and apoptosis were determined by functional experiments in vitro. Gelatin zymography assay was performed to examine MMP9 activity. In vivo, sevoflurane was injected into mice of transplantation tumor with SKOV3 cells or with pcDNA-STC1 treated SKOV3 cells. Results We found that sevoflurane inhibited the viability of SKOV3 and OVCAR3 cells in a dose-dependent manner, and colony formation assay revealed that sevoflurane inhibited ovarian cancer cell colony-formation abilities. Additionally, sevoflurane could induce cell cycle arrest and promote cell apoptosis in SKOV3 and OVCAR3 cells. Moreover, sevoflurane reduced the migration and invasion abilities of SKOV3 and OVCAR3 cells, as well as the MMP-9 activity. Furthermore, sevoflurane down-regulated the expression of stanniocalcin 1 (STC1), and up-regulation of STC1 could reverse the inhibitory effects of sevoflurane on cell proliferation and invasion. In vivo, sevoflurane significantly inhibited the tumor growth, which was be reversed by STC1 overexpression. Conclusion These data reveal an anti-cancer activity of sevoflurane on the growth and invasion of ovarian cancer, which may be through down-regulating STC1. Sevoflurane may serve as a potential anti-cancer agent in ovarian cancer therapy.

scholarly journals Multifunctional selenium nanoparticles with Galangin-induced HepG2 cell apoptosis through p38 and AKT signalling pathway

2018 ◽  
Vol 5 (11) ◽  
pp. 180509 ◽  
Author(s):  
Yinghua Li ◽  
Min Guo ◽  
Zhengfang Lin ◽  
Mingqi Zhao ◽  
Yu Xia ◽  
...  
Keyword(s):  
Hepg2 Cell ◽  
Cell Apoptosis ◽  
Hepg2 Cells ◽  
Caspase 3 ◽  
Selenium Nanoparticles ◽  
Potential Candidate ◽  
Common Cancer ◽  
Anti Cancer ◽  
Surface Decoration ◽  
Cancer Activity

The morbidity and mortality of hepatocellular carcinoma, the most common cancer, are increasing continuously worldwide. Galangin (Ga) has been demonstrated to possess anti-cancer effect, but the efficacy of Ga was limited by its low permeability and poor solubility. To develop aqueous formulation and improve the anti-cancer activity of Ga, surface decoration of functionalized selenium nanoparticles with Ga (Se@Ga) was synthesized in the present study. The aim of this study was to evaluate the anti-cancer effect of Se@Ga and the mechanism on HepG2 cells. Se@Ga-induced HepG2 cell apoptosis was confirmed by depletion of mitochondrial membrane potential, translocation of phosphatidylserine and caspase-3 activation. Furthermore, Se@Ga enhanced the anti-cancer activity of HepG2 cells through ROS-mediated AKT and p38 signalling pathways. In summary, these results suggest that Se@Ga might be potential candidate chemotherapy for cancer.

GRP137 promotes cell proliferation and metastasis through regulation of the PI3K/AKT pathway in human ovarian cancer

2018 ◽  
Vol 104 (5) ◽  
pp. 330-337 ◽  
Author(s):  
Li-qian Zhang ◽  
Su-qing Yang ◽  
Xiang-dong Qu ◽  
Xian-jun Chen ◽  
Hong-sheng Lu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
G Protein ◽  
Biological Activities ◽  
Xenograft Model ◽  
Akt Pathway ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
G Protein Coupled Receptor ◽  
Skov3 Cells ◽  
G Protein Coupled

Purpose: Ovarian cancer is one of the leading causes of death for women worldwide. The present study aims to investigate the role of G protein-coupled receptor 137 (GPR137) in the biological activities of ovarian cancer cells. Methods: (QUERY: Please supply Methods for Abstract) Results: G protein-coupled receptor 137 was highly expressed in clinical ovarian cancer tissues and exhibited the highest protein levels in SKOV3 cells and OVCAR3 cells. Knockdown of GPR137 caused significant decreases in cell proliferative rates and colony formation abilities in SKOV3 cells and OVCAR3 cells and also inhibited the in vivo tumorigenesis in a xenograft model. It was observed that knockdown of GPR137 inhibited cell motility by up to 40% in SKOV3 cells and approximately 65% in OVCAR3 cells in wound-healing assay. Cell migration abilities were consistently inhibited by 68.2% in SKOV3 cells and 59.3% in OVCAR3 cells, whereas cell invasion abilities were inhibited by 64.0% and 74.2% in SKOV3 and OVCAR3 cells, respectively, after knockdown of GPR137. When GPR137 was depleted, epithelial markers were increased, while mesenchymal markers decreased. Conclusions: Our data suggest that GPR137 plays pro-oncogenic roles in ovarian cancer via regulation of the PI3K/AKT pathway. These observations might pave new insights into therapeutic strategies against human ovarian cancer.

CHM-1 induces apoptosis via p38-mediated upregulation of DR5 expression in human ovarian cancer SKOV3 cells

2011 ◽  
Vol 670 (1) ◽  
pp. 96-104 ◽  
Author(s):  
Jang-Chang Lee ◽  
Li-Chen Chou ◽  
Chi-Hung Huang ◽  
Jing-Gung Chung ◽  
Li-Jiau Huang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Human Ovarian Cancer ◽  
Skov3 Cells

(−)-Epigallocatechin-3-Gallate (EGCG), Green Tea Component, Antagonize the Anti-Myeloma Activity of Proteasome Inhibitor PS-341 by Direct Chemical Interaction.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4850-4850 ◽  
Author(s):  
Tae Young Kim ◽  
Jongmin Park ◽  
Bora Oh ◽  
Hyun Jung Min ◽  
Tae-Sook Jeong ◽  
...  
Keyword(s):  
Synergistic Effect ◽  
Boronic Acid ◽  
Chemical Interaction ◽  
Chemotherapeutic Agents ◽  
Antagonistic Effect ◽  
Potential Candidate ◽  
Myeloma Cells ◽  
Anti Cancer ◽  
Antioxidant Function ◽  
Cancer Activity

Abstract PS-341 (also known as bortezomib, Velcade®) has a remarkable anti-myeloma acitivity and is also potential candidate for the treatment of other tumors either alone or in combination with other chemotherapeutic agents. Investigations on the effectiveness of PS-341 in combination with other anti-neoplastic agents are currently under clinical trial. Since (−)-epigallocatechin-3-gallate (EGCG) has been reported its anti-cancer activity in various cancer types, we tried a co-treatment of PS-341 with EGCG on myeloma cells, expecting a synergistic effect. However, the anti-cancer activity of PS-341 was blocked by EGCG without any synergistic effect. At the early stage of our research, we suspected antioxidant function of EGCG is the main cause of antagonistic effect on PS-341-induced cell death. Thus we selected polyphenols showing strong antioxidant function including vitamin C. But, we did not obtain any consistant data that support the significant correlation of antioxidant function of polyphenols with antagonistic effects. Instead, the structural features of polyphenols showed striking correlations with antagonistic effect; especially the presence or absence of vicinal diol moiety on polyphenol was the key elements for the effective blocking on anti-cancer function of PS-341. We infer that vicinal diols on polyphenols interact with boronic acid of PS-341, which convert active triangular boronic acid (sp2 character) of PS-341 to inactive tetrahedral boronate (sp3 character) through direct chemical interaction. The equilibrium of this conversion is controlled by structures and concentration of polyphenols, and this conversion abolished the anti-myeloma activity of PS-341. We confirmed our hypothesis on direct chemical interaction of PS-341 with EGCG through 11B NMR experiment and cell viability assay data clearly support the antagonistic interaction between PS-341 and polyphenols in multiple myeloma cell lines and primary myeloma cells from patients. Based on our researches, restriction of the intake of natural polyphenols by food or vitamin supplements should be considered during the treatment with PS-341 in MM patients. Figure Figure

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