Abstract |
The ginsenoside Rk1 is one of major components of heat-processed Panax ginseng C. A. MEYER, Sun Ginseng (SG). Here, we investigated the mechanisms underlying the anti- tumor activity of Rk1 in human hepatocellular carcinoma HepG2 cells in vitro. Rk1 markedly inhibited telomerase activity and cell growth along with significant morphological change. The expression levels of telomerase reverse transcriptase (hTERT) and c-Myc mRNA were obviously decreased with Rk1 treatment, while that of telomerase RNA (hTR) was not. Furthermore, Rk1 induced apoptosis through activation of caspases-8 and -3. However, Fas-associated death domain (FADD) expression decreased with Rk1 treatment, though it was known that the signaling cascade of FADD was associated with caspase-8 activity. Interestingly, activation of extracellular-regulated kinase (ERK) increased with Rk1 treatment. In conclusion, these results represent the first identification of the biological activity of Rk1 against HepG2 cell growth and show that the mechanism underlying the anti- tumor activity of Rk1 involves coordination between inhibition of telomerase activity and induction of apoptosis.
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Authors | Young-Joo Kim, Hak Cheol Kwon, Hyeonseok Ko, Jeong Hill Park, Hyun Young Kim, Ji-Hye Yoo, Hyun Ok Yang |
Journal | Biological & pharmaceutical bulletin
(Biol Pharm Bull)
Vol. 31
Issue 5
Pg. 826-30
(May 2008)
ISSN: 0918-6158 [Print] Japan |
PMID | 18451501
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antineoplastic Agents, Phytogenic
- Enzyme Inhibitors
- Ginsenosides
- Proto-Oncogene Proteins c-myc
- RNA, Messenger
- Reverse Transcriptase Inhibitors
- ginsenoside Rk1
- Telomerase
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Topics |
- Animals
- Antineoplastic Agents, Phytogenic
- Apoptosis
(drug effects)
- Blotting, Western
- Cell Line, Tumor
- Cell Proliferation
(drug effects)
- Cell Survival
(drug effects)
- Enzyme Inhibitors
- Flow Cytometry
- Ginsenosides
(pharmacology)
- Humans
- Liver Neoplasms, Experimental
(drug therapy, enzymology, pathology)
- Proto-Oncogene Proteins c-myc
(biosynthesis)
- RNA, Messenger
(biosynthesis)
- Reverse Transcriptase Inhibitors
- Reverse Transcriptase Polymerase Chain Reaction
- Telomerase
(antagonists & inhibitors)
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