scholarly journals Anticancer effects of novel resveratrol analogues on human ovarian cancer cells

2017 ◽  
Vol 13 (6) ◽  
pp. 1131-1141 ◽  
Author(s):  
Daniele Vergara ◽  
Stefania De Domenico ◽  
Andrea Tinelli ◽  
Eleonora Stanca ◽  
Loretta L. Del Mercato ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Anticancer Effects ◽  
Anti Cancer ◽  
Resveratrol Analogues

We describe the molecular mechanisms of the action of novel trans-restricted analogues of resveratrol with enhanced anti-cancer properties.

scholarly journals ER–Mitochondria Calcium Flux by β-Sitosterol Promotes Cell Death in Ovarian Cancer

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1583
Author(s):  
Hyocheol Bae ◽  
Sunwoo Park ◽  
Jiyeon Ham ◽  
Jisoo Song ◽  
Taeyeon Hong ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Calcium Influx ◽  
Cell Aggregation ◽  
Calcium Flux ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Anticancer Activities ◽  
Anticancer Effects ◽  
Anti Cancer

Phytosterols, which are derived from plants, have various beneficial physiological effects, including anti-hypercholesterolemic, anti-inflammatory, and antifungal activities. The anticancer activities of natural products have attracted great attention, being associated with a low risk of side effects and not inducing antineoplastic resistance. β-sitosterol, a phytosterol, has been reported to have anticancer effects against fibrosarcoma and colon, breast, lung, and prostate cancer. However, there are no reports of its activity against ovarian cancer. Therefore, we investigated whether β-sitosterol shows anticancer effects against ovarian cancer using human ovarian cancer cell lines. We confirmed that β-sitosterol induced the apoptosis of ovarian cancer cells and suppressed their proliferation. It triggered pro-apoptosis signals and the loss of mitochondrial membrane potential, enhanced the generation of reactive oxygen species and calcium influx through the endoplasmic reticulum–mitochondria axis, and altered signaling pathways in human ovarian cancer cells. In addition, we observed inhibition of cell aggregation, suppression of cell growth, and decreased cell migration in ovarian cancer cells treated with β-sitosterol. Further, our data obtained using ovarian cancer cells showed that, in combination with standard anti-cancer drugs, β-sitosterol demonstrated synergistic anti-cancer effects. Thus, our study suggests that β-sitosterol may exert anti-cancer effects against ovarian cancer in humans.

scholarly journals Anticancer Effects of Cordyceps Militaris Extract in Human Ovarian Cancer Cells via ADORA2B (P05-012-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
So Young Yoon ◽  
Soo Jung Park ◽  
Yoon Jung Park
Keyword(s):  
Ovarian Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cordyceps Militaris ◽  
Luciferase Reporter ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Camp Production ◽  
Anticancer Effects ◽  
Sch 58261

Abstract Objectives The study was aimed to determine anticancer effects of Cordyceps militaris extract (CME) and its major bioactive compound, cordycepin, in human ovarian cancer cells, and to identify their putative molecular mechanism mediated by adenosine receptors (ADORAs). Methods CME was prepared in 50% ethanol solution. LC-MS was used for quantification and Q-TOF MS for qualifying bioactive compounds in CME. MTT assay was performed for cell viability in A2780, SKOV-3, TOV112D, and OVCAR-3 human ovarian cancer cell lines. cAMP response element (CRE)-luciferase reporter gene assays were used to determine whether antitumorigenic effect of CME/cordycepin is based on adenosine derivatives. Additionally, the involvement of ADORA signaling pathway was measured using with ADORA2A antagonist SCH 58261 and ADORA2B antagonist PSB 603. Results Cordycepin concentrations of CME was 21.8%. CME was effective to reduce cell viability in A2780 and OVCAR-3 with IC50 115.2 μg/ml and 155.94 μg/ml respectively, while SKOV-3 and TOV112D were relatively resistant to CME. cAMP production was significantly increased by treatment with cordycepin and, lesser extent, with CME. Among the four types of ADORAs, ADORA2A and 2B showed relatively higher expression levels in ovarian cancer cells. The cAMP production by CME was ameliorated by PSB 603, not SCH 58261, treatment. Conclusions CME and cordycepin have anticancer effects in human ovarian cancer cells via ADORA2B-cAMP pathway. Funding Sources NRF of Korea (2017R1D1A1B03034936 & 22A20130012143) and Health Fellowship Foundation.

scholarly journals Eukaryotic initiation factor 3, subunit C silencing inhibits cell proliferation and promotes apoptosis in human ovarian cancer cells

2019 ◽  
Vol 39 (8) ◽  
Author(s):  
Fang Wen ◽  
Zhang-Ying Wu ◽  
Lei Nie ◽  
Qi-Zhu Zhang ◽  
Yuan-Kun Qin ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Molecular Mechanisms ◽  
Protein Translation ◽  
Initiation Factor ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Eukaryotic Initiation Factor ◽  
Translational Initiation

Abstract Ovarian cancer remains the leading cause of death among all gynaecological cancers, illustrating the urgent need to understand the molecular mechanisms involved in this disease. Eukaryotic initiation factor 3c (EIF3c) plays an important role in protein translation and cancer cell growth and proliferation, but its role in human ovarian cancer is unclear. Our results showed that EIF3c silencing significantly up-regulated 217 and down-regulated 340 genes. Ingenuity Pathway Analysis (IPA) indicated that the top differentially expressed genes are involved in ‘Classical Pathways’, ‘Diseases and Functions’ and ‘Networks’, especially those involved in signalling and cellular growth and proliferation. In addition, eIF3c silencing inhibited cellular proliferation, enhanced apoptosis and regulated the expression of apoptosis-associated proteins. In conclusion, these results indicate that by dysregulating translational initiation, eIF3c plays an important role in the proliferation and survival of human ovarian cancer cells. These results should provide experimental directions for further in-depth studies on important human ovarian cancer cell pathways.

scholarly journals TRPV1 Antagonist DWP05195 Induces ER Stress-Dependent Apoptosis through the ROS-p38-CHOP Pathway in Human Ovarian Cancer Cells

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1702 ◽  
Author(s):  
Yi-Yue Wang ◽  
Kyung-Tae Lee ◽  
Myong Cheol Lim ◽  
Jung-Hye Choi
Keyword(s):  
Ovarian Cancer ◽  
Cell Death ◽  
Er Stress ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Chop Expression ◽  
Anti Cancer ◽  
Trpv1 Antagonist ◽  
Induced Apoptosis

In addition to their analgesic activity, transient receptor potential vanilloid 1 (TRPV1) agonists and antagonists demonstrate profound anti-cancer activities in various human cancers. In the present study, we investigated the anti-cancer activity of a novel TRPV1 antagonist, DWP05195, and evaluated its molecular mechanism in human ovarian cancer cells. DWP05195 demonstrated potent growth inhibitory effects in all five ovarian cancer cell lines examined. DWP05195 induced apoptosis through the activation of caspase-3, -8, and -9. DWP05195 induced C/EBP homologous protein (CHOP) expression and endoplasmic reticulum (ER) stress. Sodium phenylbutyrate (4-PBA), an ER-stress inhibitor, and CHOP knockdown significantly suppressed DWP5195-induced cell death. DWP05195-enhanced CHOP expression stimulated intrinsic and extrinsic apoptotic pathways through the regulation of Bcl2-like11 (BIM), death receptor 4 (DR4), and DR5. DWP05195-induced cell death was associated with increased reactive oxygen species (ROS) levels and p38 pathway activation. Pre-treatment with the antioxidant N-acetyl-L-cysteine (NAC) significantly suppressed DWP05195-induced CHOP expression and p38 activation. Inhibition of NADPH oxidase (NOX) through p47phox knockdown abolished DWP05195-induced CHOP expression and cell death. Taken together, the findings indicate that DWP05195 induces ER stress-induced apoptosis via the ROS-p38-CHOP pathway in human ovarian cancer cells.

Gold nanoparticle-assisted enhancement in the anti-cancer properties of theaflavin against human ovarian cancer cells

2019 ◽  
Vol 104 ◽  
pp. 109909 ◽  
Author(s):  
Ritwik Maity ◽  
Manosree Chatterjee ◽  
Anmol Banerjee ◽  
Amlan Das ◽  
Raghwendra Mishra ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Gold Nanoparticle ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Anti Cancer
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