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Oncology Reports
Article
License: CC BY NC ND
Data sources: UnpayWall
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PubMed Central
Article . 2019
Data sources: PubMed Central
Oncology Reports
Article . 2019 . Peer-reviewed
Data sources: Crossref
Oncology Reports
Article . 2019
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Effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells

Authors: Zhao, Lingqin; Shou, Huafeng; Chen, Lu; Gao, Wen; Fang, Chenyan; Zhang, Ping;

Effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells

Abstract

Epigenetic modifications are closely related to oncogene activation and tumor suppressor gene inactivation. The aim of this study was to determine the effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells. Cell proliferation, metastasis, invasion and apoptosis were respectively determined using Cell Counting Kit‑8 (CCK‑8), wound healing, Transwell and flow cytometric assays. Methylation levels were determined using methylation specific PCR (MSP). Related‑factor expression was detected by conducting real‑time‑qPCR (RT‑qPCR) and western blotting. The results revealed that cell proliferation was inhibited by ginsenoside Rg3 (0, 25, 50, 100 and 200 µg/ml) in a time‑dependent manner (12, 24 and 48 h). Ginsenoside Rg3 (50, 100 and 200 µg/ml) was selected to treat cells in various experiments. When ovarian cells were treated with ginsenoside Rg3, cell apoptosis was observed to be promoted, while cell metastasis and invasion were inhibited at 48 h. The results of the present study revealed that in the promoter regions of p53, p16 and hMLH1, the methylation levels decreased, while the mRNA and protein levels significantly increased. The activities of DNMTs and mRNA as well as protein levels of DNMT1, DNMT3a and DNMT3b were decreased by Rg3. The data also demonstrated that the mRNA and protein levels of acetyl‑H3 K14/K9 and acetyl‑H4 K12/K5/K16 were increased by Rg3. Hence, ginsenoside Rg3 inhibited ovarian cancer cell viability, migration and invasion as well as promoted cell apoptosis.

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Keywords

DNA (Cytosine-5-)-Methyltransferase 1, Ovarian Neoplasms, DNA Methyltransferase 3B, Ginsenosides, Cell Survival, Apoptosis, Articles, DNA Methylation, DNA Methyltransferase 3A, Epigenesis, Genetic, Gene Expression Regulation, Neoplastic, Cell Line, Tumor, Humans, Female, DNA (Cytosine-5-)-Methyltransferases, Tumor Suppressor Protein p53, MutL Protein Homolog 1, Cyclin-Dependent Kinase Inhibitor p16, Cell Proliferation, Signal Transduction

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    selected citations
    These citations are derived from selected sources.
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    20
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Average
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
20
Top 10%
Average
Top 10%
Green
hybrid
Related to Research communities
Cancer Research