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논문 기본 정보

자료유형
학술저널
저자정보
Han-Hee Park (Ajou University School of Medicine) Seung-Won Choi (Ajou University School of Medicine) Gwang Jin Lee (Seoul National University) Young-Dae Kim (Ajou University School of Medicine) Hyun-Jin Noh (Ajou University School of Medicine) Seung-Jae Oh (Ajou University School of Medicine) Iseul Yoo (Ajou University School of Medicine) Yu-Jin Ha (Ajou University School of Medicine) Gi-Bang Koo (Ajou University School of Medicine) Soon-Sun Hong (Inha University) Sung Won Kwon (Seoul National University) You-Sun Kim (Ajou University School of Medicine)
저널정보
고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.43 No.1
발행연도
2019.1
수록면
86 - 94 (9page)

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초록· 키워드

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Background: Ginseng is believed to have antitumor activity. Autophagy is largely a prosurvival cellular process that is activated in response to cellular stressors, including cytotoxic chemotherapy; therefore, agents that inhibit autophagy can be used as chemosensitizers in cancer treatment. We examined the ability of Korean Red Ginseng extract (RGE) to prevent autophagic flux and to make hepatocellular carcinoma (HCC) cells become more sensitive to doxorubicin.
Methods: The cytotoxic effects of total RGE or its saponin fraction (RGS) on HCC cells were examined by the lactate dehydrogenase assay in a dose- or time-dependent manner. The effect of RGE or RGS on autophagy was measured by analyzing microtubule-associated protein 1A/1B-light chain (LC)3-II expression and LC3 puncta formation in HCC cells. Late-stage autophagy suppression was tested using tandem-labeled green fluorescent protein (GFP)emonomeric red fluorescent protein (mRFP)-LC3.
Results: RGE markedly increased the amount of LC3-II, but green and red puncta in tandem-labeled GFP-mRFP-LC3 remained colocalized over time, indicating that RGE inhibited autophagy at a late stage. Suppression of autophagy through knockdown of key ATG genes increased doxorubicin-induced cell death, suggesting that autophagy induced by doxorubicin has a protective function in HCC. Finally, RGE and RGS markedly sensitized HCC cells, (but not normal liver cells), to doxorubicin-induced cell death.
Conclusion: Our data suggest that inhibition of late-stage autophagic flux by RGE is important for its potentiation of doxorubicin-induced cancer cell death. Therapy combining RGE with doxorubicin could serve as an effective strategy in the treatment of HCC.

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

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UCI(KEPA) : I410-ECN-0101-2019-524-000425247