Panaxadiol, a purified ginseng component, enhances the anti-cancer effects of 5-fluorouracil in human colorectal cancer cells

Li, Xiaoli; Wang, Chong‐Zhi; Mehendale, Sangeeta R.; Sun, Shi Yong; Wang, Qi; Yuan, Chun‐Su

doi:10.1007/s00280-009-0966-0

Cited by 58 publications

(38 citation statements)

References 30 publications

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“…The protopanaxadiol group of ginsenosides are metabolised via the enteric microbiota from compound K 79 . In vitro studies suggest an enhanced effect of 5-FU against colorectal cancer cell lines in the presence of ginseng compounds 80,81 .…”

Section: [H2] Dietary Interventionsmentioning

confidence: 99%

Gut microbiota modulation of chemotherapy efficacy and toxicity

Alexander

Wilson

Teare

et al. 2017

Nat Rev Gastroenterol Hepatol

718

560

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Evidence is growing that the gut microbiota modulates the host response to chemotherapeutic drugs, with three main clinical outcomes: facilitation of drug efficacy; abrogation & compromise of anti-cancer effects, and mediation of toxicity. The implication is that gut microbiota are critical to the development of personalized cancer treatment strategies and, therefore, a greater insight into prokaryotic co-metabolism of chemotherapeutic drugs is now required. This thinking is based on evidence from human, animal and in vitro studies and gut bacteria are intimately linked to the pharmacological effects of chemotherapies (5-fluorouracil, cyclophosphamide, irinotecan, oxaliplatin, gemcitabine, methotrexate) and novel targeted immunotherapies such as anti-PD-L1 and anti-CLTA-4. The gut microbiota modulate these agents through key mechanisms, structured as the 'TIMER' mechanistic framework: namely Translocation, Immunomodulation, Metabolism, Enzymatic degradation, andReduced diversity and ecological variation The gut microbiota can now, therefore, be targeted to improve efficacy and reduce the toxicity of current chemotherapy agents. In this Review, we outline the implications of pharmacomicrobiomics in cancer therapeutics and define how the microbiota might be modified in clinical practice to improve efficacy and reduce the toxic burden of these compounds.

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Section: [H2] Dietary Interventionsmentioning

confidence: 99%

Gut microbiota modulation of chemotherapy efficacy and toxicity

Alexander

Wilson

Teare

et al. 2017

Nat Rev Gastroenterol Hepatol

718

560

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“…Cell proliferation was measured at 24, 48, and 72 h using the Cell Titer 96 Aqueous MTS Reagent (Promega, Madison, WI, USA) according to the manufacturer’s instructions. The absorbance was read by an automated microplate reader (Epoch; Bio-Tek Instruments, Winooski, VT, USA) set to a wavelength of 490 nm [16]. Data were expressed as a ratio of treated cells versus control (vehicle set at 100%).…”

Section: Methodsmentioning

confidence: 99%

Chemopreventive Effects of Oplopantriol A, a Novel Compound Isolated from Oplopanax horridus, on Colorectal Cancer

Zhang

et al. 2014

Nutrients

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Oplopanax horridus is a North American botanical that has received limited investigations. We previously isolated over a dozen of the constituents from O. horridus, and among them oplopantriol A (OPT A) is a novel compound. In this study, we firstly evaluated the in vivo chemoprevention activities of OPT A using the xenograft colon cancer mouse model. Our data showed that this compound significantly suppressed tumor growth with dose-related effects (p < 0.01). Next, we characterized the compound’s growth inhibitory effects in human colorectal cancer cell lines HCT-116 and SW-480. With OPT A treatment, these malignant cells were significantly inhibited in both a concentration- and time-dependent manner (both p < 0.01). The IC50 was approximately 5 µM for HCT-116 and 7 µM for SW-480 cells. OPT A significantly induced apoptosis and arrested the cell cycle at the G2/M phase. From further mechanism explorations, our data showed that OPT A significantly upregulated the expression of a cluster of genes, especially the tumor necrosis factor receptor family and caspase family, suggesting that the tumor necrosis factor-related apoptotic pathway plays a key role in OPT A induced apoptosis.

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“…This GE was manufactured by a steaming method which is more widely used in Asia and USA [16]. The stock solutions of GE for in vitro study were dissolved in cell culture media then filtered through 0.45 μm sterilized filter and stored at -20℃ after aliquot in 4% v/v doses.…”

Section: Methodsmentioning

confidence: 99%

Drug Interaction between Ginseng Extract (GE) and Sorafenib

Lee¹,

Park²,

Rho³

et al. 2011

Journal of Life Science

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Sorafenib is the only approved systemic, therapeutic agent for hepatocellular carcinoma (HCC). The use of Ginseng Extract (GE) in cancer patients is growing worldwide; however, drug interaction between sorafenib and GE has not been illuminated. Four different human cancer cell lines including HepG2 were used and immunocompetent mice were implanted subcutaneously with a mouse HCC cell line. Treatment with low dose GE stimulated cell growth, while a high dose inhibited growth. pERK (phosphorylation of extracellular signal-regulated kinase) was concomitantly increased and decreased respective of different doses of GE. Antitumoral effect of sorafenib decreased in non-proliferating phase cells but was sensitized after low dose GE (LDG) treatment. PD98059 (ERK phosphorylation inhibitor) efficiently blocked ERK phosphorylation, resulting in loss of sorafenib sensitization even after LDG treatment. In the HCC mouse model, LDG alone slightly increased tumor size while sorafenib alone significantly decreased it. However, a combination of LDG and sorafenib significantly decreased tumor size compared with sorafenib alone. Increase of pERK was observed in some normal mice organs and mild inflammatory change was observed in some of these organs, suggesting pERK activation by LDG may cause unexpected toxicity in normal cells. GE, dose-dependently, induced stimulation or inhibition in some human cancer cell lines. Combinational use of GE and sorafenib possibly potentiated an antitumoral response to sorafenib. pERK level has been provided as a potential predictive marker for sorafenib. Our result may suggest GE's dual effects in relation to pERK level in HCC cancer cell lines, and that certain doses of GE can sensitize sorafenib.

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Panaxadiol, a purified ginseng component, enhances the anti-cancer effects of 5-fluorouracil in human colorectal cancer cells

Abstract: Panaxadiol enhanced the anti-cancer effects of 5-FU on human colorectal cancer cells through the regulation of cell cycle transition and the induction of apoptotic cells.

Cited by 58 publications

References 30 publications

Gut microbiota modulation of chemotherapy efficacy and toxicity

Gut microbiota modulation of chemotherapy efficacy and toxicity

Chemopreventive Effects of Oplopantriol A, a Novel Compound Isolated from Oplopanax horridus, on Colorectal Cancer

Drug Interaction between Ginseng Extract (GE) and Sorafenib

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