• Asian Pacific Journal of Cancer Prevention
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• 제14권7호
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• pp.4267-4271
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• 2013

Background: As natural medicines in Asia, curcumin and triptolide extracted from different drug plants have proven to possess anticancer potential and widely used for anti-cancer research. The present study attempted to clarify that curcumin and triptolide synergistically suppress ovarian cancer cell growth in vitro. Methods: To test synergic effects, cell viability and apoptosis were analyzed after curcumin and triptolide combination treatment on ovarian cancer cell lines. Synergistic effects on apoptosis induction were determined by lactate dehydrogenase (LDH) leakage assay, intracellular reactive oxygen species (ROS) assay, mitochondrial membrane potential (MMP) loss assay and flow cytometry analysis. Critical regulators of cell proliferation and apoptosis related were analyzed by qRT-PCR and Western blotting. Results: We showed that the combination of curcumin and triptolide could synergistically inhibit ovarian cancer cell growth, and induce apoptosis, which is accompanied by HSP27 and HSP70, indicating that HSP27 and HSP70 play the important role in the synergic effect. Conclusions: From the result present here, curcumin and triptolide combination with lower concentration have a synergistic anti-tumor effect on ovarian cancer and which will have a good potential in clinical applications.

• 대한본초학회지
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• 제21권4호
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• pp.51-58
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• 2006

Objectives : In this study, we investigate that Ulmi cortex extract contributes to growth inhibitory effect and anti-cancer activity on the HT-29 human colon cancer cells. Methods : Ulmi cortex was extracted from the leaves of the plant using water. The Ulmi cortex extract was treated to different concentrations for 24 hr. Growth inhibitory effect was analyzed by measuring FACS study and MTT assay. Cell cycle inhibition was confirmed by kinases assay. Cell apoptosis was confirmed by surveying caspases cascades activation using Western blot. Results : Exposure to Ulmi cortex extract (0.4mg/ml) results in an inhibitory effect on cell growth in HT-29 cells. Growth inhibition by Ulmi cortex extract in HT-29 cells was related with the inhibition of proliferation and induction of apoptosis. The Ulmi cortex extract induces G1-cell cycle arrest and DNA fragmentation in HT-29 cells. Furthermore, Ulmi cortex extract induces cell apoptosis through the activation of caspases-3 and PARP cleavage. Conclusion : Ulmi cortex extract induces apoptosis in human colon cancer cells, therefore, we suggest that Ulmi cortex extract can be used as a novel class of anti-cancer drugs.

• Archives of Pharmacal Research
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• 제20권6호
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• pp.566-571
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• 1997

To gain further insight into how estrogens modulate cell function, the effects of estrogen on cell proliferation were studied inhuman breast cancer cells. We examined the effects of estrogen on the proliferation of three human breast cancer cell lines that differed in their estrogen receptor contents. Ten nM estradiol markedly stimulated the proliferation of MCF-7 human breast cancer cells that contained high levels of estrogen receptor $1.15{\pm}0.03 pmole/mg protein)$(over that of control. In T47D cells that contained low levels of estrogen receptor $0.23{\pm}0.05 pmole/mg protein)$, Ten nM estrogen slightly stimulated the proliferation over that of control. MDA-MB-231 cells, that contained no detectable levels of estrogen receptors, had their growth unaffected by estrogen. These results showed their sensitivity to growth stimulation by estrogen correlated well with their estrogen receptor content. Also we examined the effect of estrogen on cellular progesterone receptor level as well as plasminogen activator activity in MCF-7 cells. Ten nM estradiol showed maximal stimulation of progesterone receptor level as well as plasminogen activator activity in MCF-7 cells. It is not clear whether these stimulations of progesterone receptor and plasminogen activator activity by estrogen are related to the estrogen stimulation of cell proliferation of MCF-7 cells. Studies with estrogen in human breast cancer cells in culture indicate that sensitivity to growth stimulation by estrogen correlates well with estrogen receptor contents.

• Journal of Ginseng Research
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• 제10권2호
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• pp.141-150
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• 1986

This study was attempted to screen the cytotoxic activity of petroleum ether ex- tract from panax ginseng root against human colon cancer cells. Two extracts of panax ginseng root, crude and partially purified, were used for this experiment. The crude extract was prepared by extraction with petroleum ether using Soxhlet aparatus for 12 to 15 hours from panax ginseng and the extract was partially purified by silicic acid column with mixture of petroleum ether: ethyl ether (70 : 30, v/v). Three species of human colon cancer cells, HRT-18, HCT-48 and HT-29, were maintained in DMEM (Dulbecco's modified Eagle medium), and the cells were cultured in DMEM containing serial concentration of the crude or partially purified fraction to observe the cytotoxic activity of the both extracts. The effects of incubation time and concentration of the both extracts in culture medium against the growth of the each cancer cell were determined. The results obtained are summarized as follows: 1. The doubling times of the HRT-18, HCT-48 and HT-29 cells were about 20, 24 and 22 hours, respectively. 2, The inhibitory effects of the crude extract on the growth of cancer cells were increased according to the rise of concentration of the extract and incubation time. 3. The inhibitory effect of partially purified fraction on the growth of HRT-18 cell was about 4 times stronger than that of the crude extract under same experimental condition. 4 The inhibitory effects of the crude and purified fraction on the growth of each cancer cell were shown difference by the kind of the cancer cell. In view of the above results, it could be said that the petroleum ether extract of panax ginseng root inhibited the division of the human colon cancer cell, in vitro.

• Journal of Acupuncture Research
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• 제23권2호
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• pp.47-59
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• 2006

We previously found that cobrotoxin inhibited $NF-{\kappa}B$ activity by reacting with signal molecules of $NF-{\kappa}B$ which is critical contributor in cancer cell growth by induction of apoptotic cell death. We here investigated whether cobrotoxin inhibits cell growth of human prostate cancer cells through induction of apoptotic cell death, which is related with the suppression of the $NF-{\kappa}B$ activity. Cobrotoxin $(0{\sim}8\;nM)$ inhibited prostate cancer cell growth through increased apoptosis in a dose dependent manner. Cobrotoxin inhibited DNA binding activity of $NF-{\kappa}B$, an anti-apoptotic transcriptional factor. Consistent with the induction of apoptosis and inhibition of $NF-{\kappa}B$, cobrotoxin increased the expression of pro-apoptotic proteins caspase 3. Cobrotoxin, a venom of Vipera lebetina turanica, is a group of basicpeptides composed of 233 amino acids with six disulfide bonds formed by twelve cysteins. NF-kB is activated by subsequent release of inhibitory IkB and translocation of p50. Since sulfhydryl group is present in kinase domain of p50 subunit of NF-kB, cobrotoxin could modify NF-kB activity by protein-protein interaction. And Cobrotoxin down regulated Akt signals. Salicylic acid as a reducing agent of Sulf-hydryl group and LY294002 as a Akt inhibitor abrogated cobrotoxin-induced cell growth and DNA binding activity of $NF-{\kappa}B$. These findings suggest that nano to pico molar range of cobrotoxin could inhibit prostate cancer cell growth, and the effect may be related with the induction of apoptotic cell death through Akt dependent inhibition of $NF-{\kappa}B$ signal.

• Journal of Plant Biotechnology
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• 제46권3호
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• pp.217-227
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• 2019

Production of therapeutic monoclonal antibodies (mAbs) using a plant platform has been considered an alternative to the mammalian cell-based production system. A plant-derived mAb CO17-1AK ($mAb^P$ COK) can specifically bind to various types of cancer cell lines. The target protein of $mAb^P$ COK is the epithelial cell adhesion molecule (EpCAM) highly expressed in human epithelial cancer cells, including breast and colorectal cancer cells. It has been hypothesized that its overexpression supports tumor growth and metastasis. A ganglioside is extended well beyond the surfaces of the various cell membranes and has roles in cell growth, inflammation, differentiation, and carcinogenesis. However, the regulation of EpCAM gene expression in breast cancers and the role of gangliosides in oncogenesis are unclear. Here, the purpose of this study was to determine the effects of $mAb^P$ COK on human breast cancer cell proliferation, apoptosis, and ganglioside expression patterns. Our results show that treatment with $mAb^P$ COK suppressed the growth of breast cancer cells and induced apoptotic cell death. It also upregulated the expression of metastasis-related gangliosides in breast cancer cells. Thus, treatment with $mAb^P$ COK may have chemo-preventive therapeutic effects against human breast cancer.

• Asian Pacific Journal of Cancer Prevention
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• 제14권10호
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• pp.6089-6094
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• 2013

Berberine, a common isoquinoline alkaloid, has been shown to possess anti-cancer activities. However, the underlying molecular mechanisms are still not completely understood. In the current study, we investigated the effects of berberine on cell growth, colony formation, cell cycle distribution, and whether it improved the anticancer efficiency of cisplatin and doxorubicin in human breast cancer estrogen receptor positive (ER+) MCF-7 cells and estrogen receptor negative (ER-) MDA-MB-231 cells. Notably, berberine treatment significantly inhibited cell growth and colony formation in the two cell lines, berberine in combination with cisplatin exerting synergistic growth inhibitory effects. Accompanied by decreased growth, berberine induced G1 phase arrest in MCF-7 but not MDA-MB-231 cells. To provide a more detailed understanding of the mechanisms of action of berberine, we performed genome-wide expression profiling of berberine-treated cells using cDNA microarrays. This revealed that there were 3,397 and 2,706 genes regulated by berberine in MCF-7 and MDA-MB-231 cells, respectively. Fene oncology (GO) analysis identified that many of the target genes were involved in regulation of the cell cycle, cell migration, apoptosis, and drug responses. To confirm the microarray data, qPCR analysis was conducted for 10 selected genes based on previously reported associations with breast cancer and GO analysis. In conclusion, berberine exhibits inhibitory effects on breast cancer cells proliferation, which is likely mediated by alteration of gene expression profiles.

• Asian Pacific Journal of Cancer Prevention
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• 제14권9호
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• pp.5243-5248
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• 2013

Background: Triptolide, extracted from the herb Tripteryglum wilfordii Hook.f that has long been used as a natural medicine in China, has attracted much interest for its anti-cancer effects against some kinds of tumours in recent years. Artesunate, extracted from the Chinese herb Artemisia annua, has proven to be effective and safe as an anti-malarial drug that possesses anticancer potential. The present study attempted to clarify if triptolide enhances artesunate-induced cytotoxicity in pancreatic cancer cell lines in vitro and in vivo. Methods: In vitro, to test synergic actions, cell viability and apoptosis were analyzed after treatment of pancreatic cancer cell lines with the two agents singly or in combination. The molecular mechanisms of apoptotic effects were also explored using qRT-PCR and Western blotting. In vivo, a tumor xenograft model was established in nude mice, for assessment of inhibitory effects of triptolide and artesunate. Results: We could show that the combination of triptolide and artesunate could inhibit pancreatic cancer cell line growth, and induce apoptosis, accompanied by expression of HSP 20 and HSP 27, indicating important roles in the synergic effects. Moreover, tumor growth was decreased with triptolide and artesunate synergy. Conclusion: Our result indicated that triptolide and artesunate in combination at low concentrations can exert synergistic anti-tumor effects in pancreatic cancer cells with potential clinical applications.

• Animal cells and systems
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• 제1권2호
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• pp.389-394
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• 1997

We examined the effect of modulation of PKA isozymes on the growth of human ovarian cancer cells. Three ovarian cancer cell lines, 2774, SK-OV-3, and OVCAR-3, were examined in this study. The treatment of 5 uM 8-CI-cAMP, which has been known to down-regulate RI (or type 1 PKA) and up-regulate RII (or type II PKA), markedly inhibited the growth of all cell lines (50-80% at day 6). To test whether alteration in PKA regulatory subunits level can change the growth characteristics of ovarian cancer cells, we introduced RIIB- expression construct and Rla antisense-expression construct into 2774 cells. The overexpression of RIIB down-regulated Rla protein, and the antisense-expression of Rla up-regulated RIIB protein, showing that the intracellular levels of RI and RII are reciprocally regulated. In both cases, cell growth was reduced by 30% at day 2. These results indicate that the growth of ovarian cancer cells is controlled by the signals from PKA isozymes, and the modulation of PKA isozymes can be employed for the human ovarian cancer therapy.

• Asian Pacific Journal of Cancer Prevention
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• 제14권6호
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• pp.3987-3989
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• 2013

This is a commentary on what a cancer cell is and why cancer cells metastasize. Normal cell get transformed to a cancer cell, with excessive production of free radicals that mutate the DNA of a normal cell. The immortality and malignant stage of transformed cell is maintained by higher GSH levels. With the faster rate of proliferation, when the cancer cell finds the place of origin is not conducive to its further growth, cancer cell chooses to take the metastatic course. We argue that if we can stop the exit of cancer cell from place of origin, cancer spread can be stopped or even cured.