scholarly journals The Inhibitory Effect of Ellagic Acid on Cell Growth of Ovarian Carcinoma Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Yuan-Chiang Chung ◽  
Li-Cheng Lu ◽  
Ming-Hsiu Tsai ◽  
Yu-Jen Chen ◽  
Yi-Ying Chen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Carcinoma ◽  
Cell Lines ◽  
Ellagic Acid ◽  
Molecular Mechanisms ◽  
Inhibitory Effect ◽  
Carcinoma Cells ◽  
Dependent Manner ◽  
Ovarian Carcinoma Cells ◽  
Human Ovarian Carcinoma

Ellagic acid (EA) is able to inhibit the growth of several cancer cells; however, its effect on human ovarian carcinoma cells has not yet been investigated. Ovarian carcinoma ES-2 and PA-1 cells were treated with EA (10~100 μM) and assessed for viability, cell cycle, apoptosis, anoikis, autophagy, and chemosensitivity to doxorubicin and their molecular mechanisms. EA inhibited cell proliferation in a dose- and time-dependent manner by arresting both cell lines at the G1 phase of the cell cycle, which were from elevating p53 and Cip1/p21 and decreasing cyclin D1 and E levels. EA also induced caspase-3-mediated apoptosis by increasing the Bax : Bcl-2 ratio and restored anoikis in both cell lines. The enhancement of apoptosis and/or inhibition of autophagy in these cells by EA assisted the chemotherapy efficacy. The results indicated that EA is a potential novel chemoprevention and treatment assistant agent for human ovarian carcinoma.

Different cell cycle modulation following treatment of human ovarian carcinoma cells with a new platinum(IV) complex vs cisplatin

2007 ◽  
Vol 25 (5) ◽  
pp. 435-443 ◽  
Author(s):  
Viktor Horváth ◽  
Karel Souček ◽  
Lenka Švihálková-Šindlerová ◽  
Jan Vondráček ◽  
Olga Blanářová ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Carcinoma ◽  
Carcinoma Cells ◽  
Ovarian Carcinoma Cells ◽  
Cell Cycle Modulation ◽  
Human Ovarian Carcinoma ◽  
Human Ovarian Carcinoma Cells

scholarly journals Smad4 induces cell death in HO-8910 and SKOV3 ovarian carcinoma cell lines via PI3K-mTOR involvement

2020 ◽  
Vol 245 (9) ◽  
pp. 777-784
Author(s):  
Yushuang Yao ◽  
Zhe Zhang ◽  
Fanmao Kong ◽  
Zhuqing Mao ◽  
Zhaoyuan Niu ◽  
...  
Keyword(s):  
Cell Viability ◽  
Ovarian Carcinoma ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Treatment Strategies ◽  
Carcinoma Cells ◽  
Skov3 Cell ◽  
Ovarian Carcinoma Cells ◽  
Skov3 Cells ◽  
Induced Apoptosis

Ovarian carcinoma is one of the most common malignant cancers in women. Previous research has shown that Smad4 participates in the progression of multiple biological reactions as a crucial regulator. Nevertheless, studies on the role of Smad4 in ovarian carcinoma have been extremely limited. The study aim was to explore the mechanism underlying Smad4 regulation of HO-8910 and SKOV3 cell viability and autophagy. We observed that Smad4 gene expression in ovarian carcinoma tissues and cell lines was downregulated, and Smad4 overexpression resulted in decreased proliferation and increased autophagy in HO-8910 and SKOV3 cells (ovarian carcinoma cells). We also found that Smad4 overexpression induced apoptosis of ovarian carcinoma cells. A co-immunoprecipitation assay also revealed that Smad4 interacted with the P85 subunit of PI3K and caused its degradation and dephosphorylation. Subsequently, expression of mTOR was inhibited. Accordingly, these findings showed that further investigation of the biological mechanisms underlying ovarian carcinoma occurrence and progression is warranted, which may lead to new ovarian carcinoma treatment strategies. Impact statement This study investigated the effect and mechanism of Smad4 in ovarian carcinoma (OC) cell viability and demonstrated that Smad4 acted as a tumor suppressor in OC, which may contribute to the understanding of molecular mechanisms underlying OC occurrence and progression. Smad4 expression was decreased in the OC specimens, but Smad4 recovery in the OC cell lines impaired the survival and viability of OC cells by increasing autophagy and apoptosis. Further investigation showed that Smad4 interacted with the P85 subunit of PI3K and caused deactivation of the PI3K/mTOR pathway. Therefore, Smad4 could be considered as a target in cancer therapy due to its regulatory effect in OC carcinogenesis.

Potentiation of Azidothymidine Cytotoxicity in Cisplatin-resistant Human Ovarian Carcinoma Cells

1990 ◽  
Vol 2 (10) ◽  
pp. 339-343 ◽  
Author(s):  
Kevin J. Scanlon ◽  
Tadao Funato ◽  
Babak Pezeshki ◽  
Takeshi Tone ◽  
Lawrence C. Sowers
Keyword(s):  
Ovarian Carcinoma ◽  
Carcinoma Cells ◽  
Ovarian Carcinoma Cells ◽  
Human Ovarian Carcinoma ◽  
Human Ovarian Carcinoma Cells
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