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논문 기본 정보

자료유형
학술저널
저자정보
Hyunkyung Lee (Dongguk University-Seoul) Seungyeon Lee (Dongguk University-Seoul) Dawoon Jeong (Dongguk University-Seoul) Sun Jung Kim (Dongguk University-Seoul)
저널정보
고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.42 No.4
발행연도
2018.10
수록면
455 - 462 (8page)

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Background: Ginsenoside Rh2 has been known to enhance the activity of immune cells, as well as to inhibit the growth of tumor cells. Although the repertoire of genes regulated by Rh2 is well-known in many cancer cells, the epigenetic regulation has yet to be determined, especially for comprehensive approaches to detect methylation changes.
Methods: The effect of Rh2 on genome-wide DNA methylation changes in breast cancer cells was examined by treating cultured MCF-7 with Rh2. Pyrosequencing analysis was carried out to measure the methylation level of a global methylation marker, LINE1. Genome-wide methylation analysis was carried out to identify epigenetically regulated genes and to elucidate the most prominent signaling pathway affected by Rh2. Apoptosis and proliferation were monitored to examine the cellular effect of Rh2.
Results: LINE1 showed induction of hypomethylation at specific CpGs by 1.6e9.1% (p < 0.05). Genomewide methylation analysis identified the “cell-mediated immune response”-related pathway as the top network. Cell proliferation of MCF-7 was retarded by Rh2 in a dose-dependent manner. Hypermethylated genes such as CASP1, INSL5, and OR52A1 showed downregulation in the Rh2-treated MCF-7, while hypomethylated genes such as CLINT1, ST3GAL4, and C1orf198 showed upregulation. Notably, a higher survival rate was associated with lower expression of INSL5 and OR52A1 in breast cancer patients, while with higher expression of CLINT1.
Conclusion: The results indicate that Rh2 induces epigenetic methylation changes in genes involved in immune response and tumorigenesis, thereby contributing to enhanced immunogenicity and inhibiting the growth of cancer cells.

목차

abstract
1. Introduction
2. Materials and methods
3. Results
4. Discussion
References

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