• Analytical Science and Technology
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• v.31 no.6
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• pp.232-239
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• 2018

Human breast milk (HBM) provides neonates with indispensable nutrition. The present study evaluated the anti-cancer activity of diluted and pasteurized early HBM (< 6 weeks' lactation) on human breast cancer cell lines. The cell lines MCF7 and MDA-MB231 were exposed to 1 % HBM from the 1st, 3rd, and 6th weeks of lactation and exhibited reduced proliferation rates. As controls, breast cell lines (293T and MCF-10A), breast cancer cell lines (MCF-7 and MDA-MB-231), and $CD133^{hi}CXCR4^{hi}ALDH1^{hi}$ patient-derived human cancer stem-like cells (KU-CSLCs) were treated with prominent milk proteins ${\beta}$-casein, ${\kappa}$-casein, and lactoferrin at varying doses (10, 50, and $100{\mu}g$) for 24 or 48 hrs. The impact of these proteins on cell proliferation was investigated. Breast cancer cell lines treated with ${\kappa}$-casein and lactoferrin exhibited significantly reduced viability, in both a dose- and time-dependent manner. Interestingly, ${\kappa}$-casein selectively impacted only cancer (but not normal breast) cell lines, particularly the more malignant cell line. However, ${\beta}$-casein-exposed human breast cancer cell lines exhibited a significantly higher proliferation rate. Thus, ${\kappa}$-casein and lactoferrin appear to exert selective anti-cancer activities. Further studies are warranted to determine the mechanisms underlying ${\kappa}$-casein- and lactoferrin-mediated cancer cell-selective cytotoxic effects.

• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.4
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• pp.691-695
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• 2002

This study was performed to examine the cytotoxic effects of the distilled pine-needle extracts against several cancer cell lines. First, cell lines including mice leukemic cancer cell line (L1210), sarcoma 180 and human monocyte-like cancer cells (U937) were tested using XTT methods in uitro. Pine-needle extracts were prepared by pressing the pine needles and distilling it at below 98$^{\circ}C$ and then added to the growth medium in a final dilution of 10, 20, and 40 times. Growth of three kinds of cancer cells was significantly inhibited by more than 50% with the addition of the extracts. Fifty six to seventy six % of inhibition was shown with the 40 times dilution of the extracts. Greater inhibition was achieved with the 20 times dilution (81~90%) and the 10 times dilution (77~89%) of the extracts. Next, other human cancer cell lines including 3 kinds of breast cancer cell lines (T47D, MDA-MB-231 and MW7A) and one hepatoma cell line (SNU-354) were tested with the 20 times dilution of the extract. T47D and MDA-MB-231 cell lines showed lower inhibition (12%) with the addition of the extract. However, MH7A and SNU-354 cell lines showed 64% and 72% inhibition with the extract, respectively. These results suggest that the distilled pine-needle extracts have strong cytotoxic effect on certain cancer cell lines and the intensity of the effect may vary depending on the process of the pine needle.

• Journal of Chest Surgery
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• v.39 no.9 s.266
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• pp.668-673
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• 2006

Background: Docetaxel has been effectively used as an anti-cancer chemotherapuetic agent for various tumor treatments including lung cancer. However, the cell death induction mechanism(s) involved with docetaxel treatment in lung cancer cells has not been known yet. Material and Method: In the present study, the cellular and biochemical changes of NCI-H1703 cells (non-small cell lung cancer cell line, p53-mutant) after docetaxel treatment have been monitored by flow cytometry, fluorescence microscopy and western blot. Result: Docetaxel treatment significantly resulted in decrease of S phase as well as increase of G2 phase, and consequently evoked an increase of cell death in NCI-H1703 cells. After docetaxel exposure the activations of caspase-3 and caspase-9 were detected. Conclusion: Take together, it is suggested that the docetaxel induces NCI-H1703 cell death by caspase-9 and caspase-3 dependent mitochondrial apoptotic pathway.

• BMB Reports
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• v.47 no.5
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• pp.274-279
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• 2014

Bortezomib has been known as the most promising anti-cancer drug for multiple myeloma (MM). However, recent studies reported that not all MM patients respond to bortezomib. To overcome such a stumbling-block, studies are needed to clarify the mechanisms of bortezomib resistance. In this study, we established a bortezomib-resistant cell line (U266/velR), and explored its biological characteristics. The U266/velR showed reduced sensitivity to bortezomib, and also showed cross-resistance to the chemically unrelated drug thalidomide. U266/velR cells had a higher proportion of CD138 negative subpopulation, known as stem-like feature, compared to parental U266 cells. U266/velR showed relatively less inhibitory effect of prosurvival NF-${\kappa}B$ signaling by bortezomib. Further analysis of RNA microarray identified genes related to ubiquitination that were differentially regulated in U266/velR. Moreover, the expression level of CD52 in U266 cells was associated with bortezomib response. Our findings provide the basis for developing therapeutic strategies in bortezomib-resistant relapsed and refractory MM patients.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.sup3
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• pp.293-297
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• 2016

TRAIL, tumor necrosis factor (TNF)-related apoptosis-inducing ligand belongs to one of important cytokine superfamilIES, tumor necrosis factor ($TNF{\alpha}$). TRAIL-2 receptor agonists activate several cell signaling pathways in cells in different manners and could lead to apoptosis or necrosis. Agonistic egg yolk antibodies like IgY which have been developed in a selective manner could activate TRAIL death receptors such as TRAIL-2 (DR5) and thus apoptosis signaling. We here investigated induction of apoptosis in human breast cancer cells (MCF7 cell line) by an IgY produced against an 21 aminoacid epitope of the human TRAIL-2 receptor. As the first step a small peptide of 21 aminoacids choosen from the extracellular domain of DR5 protein was produced with a peptide synthesizer. After control assays and confirmation of the correct amino acid sequence, it was injected to hens immunized to achieve high affinity IgYs. At the next step, the produced IgYs were extracted and examined for specificity against DR5 protein by ELISA assay. Subsequently, the anticancer effect of such IgYs was determined by MTT assay in the MCF7 human breast cancer cell line. The produced peptides successfully immunized hens and the produced antibodies which accumulated in egg yolk specifically recognized the DR5 protein. IgYs exerted significant toxicity and killed MCF7 cells as shown by MTT assay.

• Tuberculosis and Respiratory Diseases
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• v.58 no.5
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• pp.465-472
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• 2005

Background : The survival benefit associated with first-line chemotherapy in lung cancer has led to the need for second-line chemotherapy, for which Docetaxel ($Taxotere^{(R)}$) has proven efficacy in both settings. This study evaluated the safety and efficacy of docetaxel in patients with non-small cell lung cancer who had failed first-line platinum-based chemotherapy. Methods : Thirty one patients with non-small-cell lung cancer, who had failed first-line platinum-based chemotherapy, between March 1999 and August 2003, were enrolled in this study. Patients received intravenous docetaxel, either $75mg/m^2$ or $100mg/m^2$, with routine premedication every three weeks. Results : Fourteen patients (45.2%) had a partial response. The median survival and progression-free survival times were 12.5 months (95% CI 7.3-17.6) and 3.0 months (95% CI 1.6-4.5), respectively. This study showed 2 factors gave different survival benefits; the age (< 60 years: 20.1 months vs. ${\geq}60years$: 6.6 months, p = 0.0105) and the histological type (adenocarcinoma: 25.6 months vs. others: 7.9 months, p=0.0055). The predominant toxicity was neutropenia, which occurred as WHO grade 3 or 4 in 38.7 % of patients. One treatment-related death was also reported. Non-hematological toxicity was minor and easily controlled. There were no significant statistical differences in the survival benefit and toxicity between the two doses. Conclusion : Docetaxel, as second-line monotherapy, was well tolerated and effective in patients with non-small-cell lung cancer who failed first-line platinum-based chemotherapy.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.3
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• pp.1403-1410
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• 2014

Epigenetic regulators like histone deacetylases (1 and 2), and viral onco-proteins (E6/E7) are known to be overexpressed in cervical cancer cells. The present study was designed to investigate the effect of curcumin on HDACs (1 and 2) and HPV E6/E7 in the cervical cancer cell line SiHa and a drug resistant clone $SiHa^R$ (derived from SiHa). It was further intended to investigate whether curcumin could sensitize the cells towards cisplatin induced cell killing by modulation of multi drug resistant proteins like MRP1 and Pgp1. Curcumin inhibited HDACs, HPV expression and differentially increased acetylation and up-regulation of p53 in SiHa and $SiHa^R$, leading to cell cycle arrest at G1-S phase. Up-regulation of pRb, p21, p27 and corresponding inhibition of cyclin D1 and CDK4 were observed. Cisplatin resistance in $SiHa^R$ due to over-expression of MRP1 and Pgp1 was overcome by curcumin. Curcumin also sensitized both the cervical cancer cells towards cisplatin induced cell killing. Inhibition of HDACs and HPVs led to cell cycle arrest at G1/S phase by alteration of cell cycle regulatory proteins. Suppression of MRP1 and Pgp1 by curcumin resulted in sensitization of cervical cancer cells, lowering the chemotherapeutic dose of the drug cisplatin.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.9
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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.

• BMB Reports
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• v.41 no.11
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• pp.803-807
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• 2008

We investigated the expression of muscarinic acetylcholine receptors (mAChRs) and their possible involvement in the regulation of cell proliferation in four colon cancer cell lines (SNU-61, SNU-81, SNU-407, and SNU-1033) derived from Korean colon carcinoma patients. A ligand binding assay showed that all four cell lines expressed mAChRs. Treatment of the four cell lines with the cholinergic agonist carbachol led to the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2). In SNU-407 cells, carbachol significantly stimulated cell proliferation, which could be abolished by the muscarinic antagonist atropine and the ERK1/2 kinase inhibitor PD98059. These results indicate that mAChRs specifically mediate the proliferation of SNU-407 colon cancer cells via the ERK1/2 pathway.

• The Journal of Korean Medicine
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• v.19 no.1
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• pp.327-338
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• 1998

To investigate effect of water extract of PaIMuITang(PMT) on human cancer cell-lines and immunocytes, this research estimated proliferation of A431 cell line, KHOS-NP cell line, mouse thymocytes and mouse splenocytes, Nitric Oxide(NO) from macrophage, apoptosis and subpopulation of the mouse thymocytes. The results were obtained as follows; 1. PMT inhibited the. proliferation of A431 cell line, but it is not significant. 2. PMT inhibited the proliferation of KHOS-NP cell line, but it is not significant. 3. PMT stimulated the proliferation of mouse thymocytes, being compared Con A non-treated group. 4. PMT stimulated the proliferation of mouse splenocytes, being compared LPS treated group. 5. PMT l00g/mQ inhibited the production of NO from macrophages in vitro, being compared NPS IFN treated group. 6. PMT inhibited the production of NO from macrophages in vivo, being compared LPS|IFN treated group. 7. PMT accelerated the induction of apoptosis of the mouse thymocytes. 8. In subpopulation PMT decreased $T_H$ of the mouse thymocytes, but increased T /dT s of the mouse thymocytes.