• Journal of Physiology & Pathology in Korean Medicine
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• v.26 no.5
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• pp.687-692
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• 2012

Schizandra chinensis extract has been known to possess a variety of efficacy including antitumor. However, it remains unclear how schizandrin, which is a major biological active ingredient of Schizandra chinensis, exerts antitumor effect. This study was designed to investigate the mechanism by which schizandrin inhibits tumor growth and metastasis. In in vivo test using tumor model mice injected with B16BL6 cell line, mice treated with 10 and 100 ${\mu}g/ml$ schizandrin showed a significant inhibition by $73.79{\pm}6.43%$ and $90.46{\pm}1.72%$, respectively, compared with positive tumor controls. Schizandrin did not exert a significant toxicity for the normal cells (HUVECs) and tumor cell lines (A549, B16BL6, Du145, Huh7). Treatment with schizandrin at 10 and 100 ${\mu}g$/head significantly inhibited the tumor-induced angiogenesis by $68.04{\pm}32.21%$ and $103.8{\pm}34.99%$ compared with the positive control group, respectively. Using in vivo lung metastasis model, tumor metastasis assay revealed that 10 and 100 ${\mu}g$/head schizandrin significantly decreased the metastatic lung tumor by $37.51{\pm}8.15%$ and $75.53{\pm}4.38%$ compared with positive controls, respectively. On the other hand, schizandrin did not affect the adherence of B16BL6 cell line to extracellular matrix protein. These results demonstrate that schizandrin exerts inhibitory effect on tumor growth and metastasis by inhibiting angiogenesis. This study thus suggest that schizandrin may be a candidate molecule target for cancer drug development.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.4
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• pp.856-859
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• 2007

We have investigated the antimetastatic and antitumor effects of Ginsenoside Rh2 and ${\beta}-glucan$ unsing an experimental metastatic mouse model intravenously injected with B 16 melanoma F 10 cells. Animal groups are divided into six groups according to the dosage of drug administration and the kind of drugs. The groups are control, ${\beta}-glucan$ with 50, 100 and 200 mg/kg, Geinsenoside Rh2 50 mg/kg, and ${\beta}-glucan$ 50 mg/kg + Ginsenoside Rh2 50 mg/kg. Oral administration of various concentration of ${\beta}-glucan$( 50, 100, and 200 mg/kg) were reduced the lung- metastatics induced by metastatic B16 melanoma F 10 cells injection with a dose dependent manner in the syngenic mice. At same dosage group, Ginsenoside Rh2 (50 mg/kg) has more antimetastatic effect than the ${\beta}-glucan$(50 mg/kg). The highest antimetastatic effects was observed in the ${\beta}-glucan$ 50 mg/kg + Ginsenoside Rh2 50 mg/kg group and has a similar tendency in the anti-tumor effects, including decrease of the average tumor weight and increase of the average survival rate. There are no differences of the average tumor weights were apparent in the ${\beta}-glucan$ groups, however there were little decrease of the average tumor weight in Ginsenoside 50 mg/kg group and ${\beta}-glucan$ 50 mg/kg + Ginsenoside Rh2 50 mg/kg group than that of the control group. The rate of average survival rate in the ${\beta}-glucan$ 50 mg/kg + Ginsenoside Rh2 50 mg/kg group, ${\beta}-glucan$ 200 mg/kg, ${\beta}-glucan$ 100 mg/kg and ${\beta}-glucan$ 50 mg/kg, and Ginsenoside 50 mg/kg groups were highly in order. These data suggest that antimetastatic and antitumor effect of combination of Ginsenodide Rh2 and ${\beta}-glucan$ be the highest in this study.

• Archives of Pharmacal Research
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• v.26 no.10
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• pp.861-867
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• 2003

Inhibitory effect of the lectins (KML-C) isolated from Korean mistletoe (KM; Viscum album coloratum) on tumor metastases produced by murine tumor cells (B16-BL6 melanoma, colon 26M3.1 carcinoma and L5178Y-ML25 lymphoma cells) was investigated in syngeneic mice. An intravenous (i.v.) administration of KML-C (20-50 ng/mouse) 2 days before tumor inoculation significantly inhibited lung metastases of both B16-BL6 and colon 26-M3.1 cells. The prophylactic effect of 50 ng/mouse of KML-C on lung metastasis was almost the same with that of 100 $\mu$ g/mouse of KM. Treatment with KML-C 1 day after tumor inoculation induced a significant inhibition of not only the experimental lung metastasis induced by B16-BL6 and colon 26M3.1 cells but also the liver and spleen metastasis of L5178Y-ML25 cells. Furthermore, multiple administration of KML-C given at 3 day-intervals after tumor inoculation led to a significant reduction of lung metastasis and suppression of the growth of B16-BL6 melanoma cells in a spontaneous metastasis model. In an assay for natural killer (NK) cell activity. i.v. administration of KML-C (50 ng/mouse) significantly augmented NK cytotoxicity against Yac-1 tumor cells 2 days after KML-C treatment. In addition, treatment with KML-C (50 ng/mouse) induced tumoricidal activity of peritoneal macrophages against B16-BL6 and 3LL cells. These results suggest that KML-C has an immunomodulating activity to enhance the host defense system against tumors, and that its prophylactic and therapeutic effect on tumor metastasis is associated with the activation of NK cells and macrophages.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.2
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• pp.412-415
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• 2009

Chinensis galla has been used as an multi-functional herb, such as anti-inflammatory, anti-virus, and antitumor agent. This study was performed to antimicrobial and cytotoxicity effect in vitro. The results were summarized as follows : Chinensis galla was antimicrobial effect on Staphylococcus aureus subsp. aureus, Bacillus cereus, Bacillus subtilis, Staphylococcus epidermidis. Chinensis galla was antimicrobial effect on Kocuria rhizophila, Corynebacterium ammoniagenes. The extracts of Chinensis galla exhibited cytotoxicity on human dermal fibroblast at $10\;{\mu}{\ell}$ but not at $5\;{\mu}{\ell}$, and the same results was known under a microscope. Accordingly the results show Chinensis galla could antimicrobial effect but exhibited cytotoxicity on human dermal fibroblast at high concentration and it needs more research.

• Biomolecules & Therapeutics
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• v.23 no.3
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• pp.225-232
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• 2015

We identified a novel Akt signaling mechanism that mediates fucoidan-induced suppression of human colon cancer cell (HT29) proliferation and anticancer effects. Fucoidan treatment significantly inhibited growth, induced G1-phase-associated upregulation of p21WAF1 expression, and suppressed cyclin and cyclin-dependent kinase expression in HT29 colon cancer cells. Additionally, fucoidan treatment activated the Akt signaling pathway, which was inhibited by treatment with an Akt inhibitor. The inhibition of Akt activation reversed the fucoidan-induced decrease in cell proliferation, the induction of G1-phase-associated p21WAF1 expression, and the reduction in cell cycle regulatory protein expression. Intraperitoneal injection of fucoidan reduced tumor volume; this enhanced antitumor efficacy was associated with induction of apoptosis and decreased angiogenesis. These data suggest that the activation of Akt signaling is involved in the growth inhibition of colon cancer cells treated with fucoidan. Thus, fucoidan may serve as a potential therapeutic agent for colon cancer.

• Biomolecules & Therapeutics
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• v.5 no.2
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• pp.215-221
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• 1997

In an effort to screen new selective antitumor agents from the broth of soil microorganism, cytotoxicity oriented screening was performed against tumor cells and 3 compounds (Compound 1, 2 and 3) were isolated from Sreptomyces parvullus ISP 5048 and their chemical structures were determined. Among these compounds, Compound 2 showed the highest cytotoxicity against P388Dl and L1210. While the $IC_{50}$/ values of compound 2 against P388Dl and L1210 were 0.073$\mu$g/ml and 0.07$\mu$g/ml, respectively, and the $IC_{50}$/ value of Compound 3 was 0.17$\mu$g/ml against human lung cancer cells, A549, the cytotoxicity of Compound 2 and 3 against normal cell line, Vero E6 cell was about 4- and 8-fold lower than that of adriamycin. Based on the chemical analysis data, Compound 3 was octacosamicine A, a known antibiotic, which was reported by Dobasih et al. (1988). Taken together the results demonstrated that Compound 2 and Compound 3 has the possibility to be developed as antitumor agent because of its potent cytotoxicity as well as high selectivity against various cancer cell lines.

• The Journal of Korean Medicine
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• v.20 no.2
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• pp.128-140
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• 1999

To evaluate the antitumor activity, antimetastatic and immunomodulatory effects of samryongbakchulsankamibang(SBSK) studies were done experimentally, In cytotoxicity against P388, A549. SK-OV-3, B16-F10 and SK-MEL-2. concentration inhibiting cell growth up to below 40% of control was recognized at $10^{-3}g/ml$ of SBSK. In Inhibitory effect on activity of DNA topoisomerase I. the $IC_{50}$ was shown $200-400{\mu}g/ml$ of SBSK. The T/C was 154% in SBSK-treated group in S-180 bearing ICR mice, The concentration inhibiting adhesion of A549 and B16-F10 to complex extracellular matrix up to below 30% of control was recognized at $5{\times}10^{-4}$, $1{\times}10^{-3}\;g/ml$ of SBSK. In pumonary colonization assay with B16-BL/6, a number of colonies in the lungs were decreased significantly in SBSK-treated group as compared with control group, In hematological changes in B16-BL/6 injected C57BL/6, numbers of WBC and platelet were not changed significantly in SBSK-treated groups, In CAM and in vitro neovascularization assay, angiogenesis was inhibited significantly in SBSK-treated group as compared with control group. From above results it was concluded that SBSK could be usefully applied for the prevention and treatment of cancer.

• Biotechnology and Bioprocess Engineering:BBE
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• v.9 no.5
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• pp.356-361
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• 2004

When SiHa cells were incubated for varying periods of time with extracts of PFF and PFM, the cytotoxicity of the ethanol extracts of PFF was higher than those of the other extracts. These results indicated that the extracts from fruiting bodies of p. ferulae contain antitumor Substances. When A549, SiHa and HeLa cells were incubated with different concentrations of PFF and PFM extracts, the ethanol extracts of PFF showed strong cytotoxicity against A549 tells at concentrations over $10{\mu}g/mL$ and against SiHa and HeLa cells at concentrations over $40{\mu}g/mL$. However, the differences in the cytotoxic effects of the hot water and ethanol extracts of PFM and the hot water extracts of PFF on all 3 cancer cells were not significant. Also, the PFF ethanol extracts induced synergistic effects on the TRAIL-induced apoptosis in A549 cells, which were strongly resistant to TRAIL. These results indicated that ethanol extracts of PFF were the most prominent antitumor agents toward lung cancer cells (A549).

• Biomedical Science Letters
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• v.24 no.1
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• pp.15-22
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• 2018

Pristimerin is a triterpene compound isolated from plant extracts that reportedly possesses antitumor, antioxidant, and anti-inflammatory activities. The current study was designed to evaluate the antitumor effects of pristimerin on human colon cancer cells. Treatment of the human colon cancer cells, HCT116 and SW480, with pristimerin led to a dose-dependent decrease in cell proliferation. Flow cytometry experiments showed that pristimerin increased cell apoptotic rate and decreased the mitochondrial membrane potential in HCT116 and SW480 cells. Western blot assay showed that pristimerin induced increased cleavage of caspase-3, -7, -8, and poly ADP ribose polymerase. Treatment with pristimerin also caused a marked decrease in the expression of Bcl-2 and Bcl-xL. Additionally, the levels of phosphorylated AKT and forkhead box O3a (FOXO3a) were decreased in pristimerin-treated colon cancer cells. Taken together, our study illustrated that pristimerin promoted apoptosis via the AKT/FOXO3a signaling pathway in colon cancer cells, elucidating that it might be considered as a potential agent for colon cancer therapy.

• Animal cells and systems
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• v.13 no.2
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• pp.113-118
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• 2009

Extracts derived from various medical mushrooms have been reported to have antitumor and immuno-modulatory properties. In order to investigate the antitumor activity of keumsa Linteusan, the water extract of Phellinus Iimteus, HT1080 cells, a human fibrosarcoma cell line, were treated with it and changes in cellular migration potential was tested in vitro. At a concentration range below 1,000 $\mu$g/mL, Linteusan blocked, in a dose dependent manner, the migration of cells through Matrigel as well as Boyden chamber without affecting the viability of the cells. Prolonged treatment of HT1080 cells with Linteusan suppressed TNFa induced production of matrix metalloproteinase (MMP)-9 as well as basal level expression of MMP-2. Linteusan also affected the adhesion of the cells to fibronectin-coated surfaces. The effect of Linteusan on cell signaling pathways was also tested. Linteusan specifically affected TNF-$\alpha$ induced phosphorylation of AKT in a dose-dependent manner, while phosphorylation levels of ERK remained unaffected. These data indicate that Linteusan blocks the migration of HT1080 cells by affecting various processes associated with cell migration such as the expression of matrix degradingenzymes,cell adhesion, and AKT-medicated cellular signaling pathways.