Please use this identifier to cite or link to this item:
https://doi.org/10.18632/oncotarget.2034
DC Field | Value | |
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dc.title | 20(S)-Ginsenoside Rg3 is a novel inhibitor of autophagy and sensitizes hepatocellular carcinoma to doxorubicin | |
dc.contributor.author | Kim, D.-G | |
dc.contributor.author | Jung, K.H | |
dc.contributor.author | Lee, D.-G | |
dc.contributor.author | Yoon, J.-H | |
dc.contributor.author | Choi, K.S | |
dc.contributor.author | Kwon, S.W | |
dc.contributor.author | Shen, H.-M | |
dc.contributor.author | Morgan, M.J | |
dc.contributor.author | Hong, S.-S | |
dc.contributor.author | Kim, Y.-S | |
dc.date.accessioned | 2020-10-28T07:12:20Z | |
dc.date.available | 2020-10-28T07:12:20Z | |
dc.date.issued | 2014 | |
dc.identifier.citation | Kim, D.-G, Jung, K.H, Lee, D.-G, Yoon, J.-H, Choi, K.S, Kwon, S.W, Shen, H.-M, Morgan, M.J, Hong, S.-S, Kim, Y.-S (2014). 20(S)-Ginsenoside Rg3 is a novel inhibitor of autophagy and sensitizes hepatocellular carcinoma to doxorubicin. Oncotarget 5 (12) : 4438-4451. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.2034 | |
dc.identifier.issn | 19492553 | |
dc.identifier.uri | https://scholarbank.nus.edu.sg/handle/10635/181780 | |
dc.description.abstract | Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide. High mortality from HCC is mainly due to widespread prevalence and the lack of effective treatment, since systemic chemotherapy is ineffective, while the targeted agent Sorafenib extends median survival only briefly. The steroidal saponin 20(S)-ginsenoside Rg3 from Panax ginseng C.A. Meyer is proposed to chemosensitize to various therapeutic drugs through an unknown mechanism. Since autophagy often serves as cell survival mechanism in cancer cells exposed to chemotherapeutic agents, we examined the ability of Rg3 to inhibit autophagy and chemosensitize HCC cell lines to doxorubicin in vitro. We show that Rg3 inhibits late stage autophagy, possibly through changes in gene expression. Doxorubicin-induced autophagy plays a protective role in HCC cells, and therefore Rg3 treatment synergizes with doxorubicin to kill HCC cell lines, but the combination is relatively nontoxic in normal liver cells. In addition, Rg3 was well-tolerated in mice and synergized with doxorubicin to inhibit tumor growth in HCC xenografts in vivo. Since novel in vivo inhibitors of autophagy are desirable for clinical use, we propose that Rg3 is such a compound, and that combination therapy with classical chemotherapeutic drugs may represent an effective therapeutic strategy for HCC treatment. | |
dc.rights | Attribution 4.0 International | |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
dc.source | Unpaywall 20201031 | |
dc.subject | autophagy protein 5 | |
dc.subject | bafilomycin A1 | |
dc.subject | caspase 3 | |
dc.subject | chloroquine | |
dc.subject | cycloheximide | |
dc.subject | death receptor 5 | |
dc.subject | doxorubicin | |
dc.subject | ginsenoside Rg 3 | |
dc.subject | growth arrest and DNA damage inducible protein 153 | |
dc.subject | LC3 II protein | |
dc.subject | membrane protein | |
dc.subject | protein p62 | |
dc.subject | unclassified drug | |
dc.subject | antineoplastic antibiotic | |
dc.subject | doxorubicin | |
dc.subject | ginsenoside | |
dc.subject | ginsenoside Rg 3 | |
dc.subject | adjuvant therapy | |
dc.subject | animal cell | |
dc.subject | animal experiment | |
dc.subject | animal model | |
dc.subject | animal tissue | |
dc.subject | article | |
dc.subject | autophagosome | |
dc.subject | autophagy | |
dc.subject | cancer combination chemotherapy | |
dc.subject | cancer inhibition | |
dc.subject | cell death | |
dc.subject | chemosensitization | |
dc.subject | controlled study | |
dc.subject | dose time effect relation | |
dc.subject | drug effect | |
dc.subject | drug efficacy | |
dc.subject | drug inhibition | |
dc.subject | drug mechanism | |
dc.subject | drug potentiation | |
dc.subject | drug response | |
dc.subject | drug tolerability | |
dc.subject | enantiomer | |
dc.subject | enzyme activation | |
dc.subject | gene expression | |
dc.subject | ginseng | |
dc.subject | in vitro study | |
dc.subject | in vivo study | |
dc.subject | liver cell carcinoma | |
dc.subject | male | |
dc.subject | mouse | |
dc.subject | nonhuman | |
dc.subject | protein cleavage | |
dc.subject | protein stability | |
dc.subject | tumor volume | |
dc.subject | tumor xenograft | |
dc.subject | upregulation | |
dc.subject | autophagy | |
dc.subject | Carcinoma, Hepatocellular | |
dc.subject | female | |
dc.subject | human | |
dc.subject | Liver Neoplasms | |
dc.subject | Antibiotics, Antineoplastic | |
dc.subject | Autophagy | |
dc.subject | Carcinoma, Hepatocellular | |
dc.subject | Doxorubicin | |
dc.subject | Female | |
dc.subject | Ginsenosides | |
dc.subject | Humans | |
dc.subject | Liver Neoplasms | |
dc.subject | Male | |
dc.type | Article | |
dc.contributor.department | PHYSIOLOGY | |
dc.description.doi | 10.18632/oncotarget.2034 | |
dc.description.sourcetitle | Oncotarget | |
dc.description.volume | 5 | |
dc.description.issue | 12 | |
dc.description.page | 4438-4451 | |
Appears in Collections: | Staff Publications Elements |
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