• Molecules and Cells
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• v.42 no.9
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• pp.628-636
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• 2019

Altered genetic features in cancer cells lead to a high rate of aerobic glycolysis and metabolic reprogramming that is essential for increased cancer cell viability and rapid proliferation. Pyruvate kinase muscle (PKM) is a rate-limiting enzyme in the final step of glycolysis. Herein, we report that PKM is a potential therapeutic target in triple-negative breast cancer (TNBC) cells. We found that PKM1 or PKM2 is highly expressed in TNBC tissues or cells. Knockdown of PKM significantly suppressed cell proliferation and migration, and strongly reduced S phase and induced G2 phase cell cycle arrest by reducing phosphorylation of the CDC2 protein in TNBC cells. Additionally, knockdown of PKM significantly suppressed $NF-{\kappa}B$ (nuclear factor kappa-light-chain-enhancer of activated B cells) activity by reducing the phosphorylation of p65 at serine 536, and also decreased the expression of $NF-{\kappa}B$ target genes. Taken together, PKM is a potential target that may have therapeutic implications for TNBC cells.

• The Journal of Internal Korean Medicine
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• v.27 no.1
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• pp.149-165
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• 2006

Objectives: This study was done to evaluate the effects of Saengkankunbi-tang on cell-viability, proliferation, cell-cycle, apoptosis and DNA replication on HepG2 cell and to find out by which molecular-biological mechanism by which Saengkankunbi-tang operates. Methods : The MTT assay, cell counting assay, [3H]-thymidine incorporation assay, flow cytometric analysis, tryphan blue exclusion assay, western blot analysis, quantative RT-PCR were taken. Results : Saengkankunbi-tang had no effect on proliferation, cell-cycle and DNA replications of HepG2 cells, while it improved cell viability and reduced apoptosis, and it activated Akt and NFKB. But, it did not produce an effect on cell viability and apoptosis when P13K/Akt pathway was blocked by LY294002 nor when $NF{\kapa}B$ activation was blocked by DN-$I{\kapa}B$. Conclusion : These results suggests that Saengkankunbi-tang improves cell viability and reduces apoptosis of HepG2 cells, by activating $NF{\kapa}B$ through PI3K/Akt pathway.

• Journal of Korean Neurosurgical Society
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• v.37 no.1
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• pp.70-72
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• 2005

Primary spinal cord lymphomas are rare, and are either extra-/intradural masses with leptomeningeal infiltration or intramedullary in nature. The authors present a patient with a diffuse large B-cell lymphoma involving the sacral nerve root, extension to extradural space, and the cranial nerve.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.210.1-210.1
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• 2003

In this study, we investigated the effect of inhibition of proliferation and antioxidant effect on B16F10 murine melanoma cell. Also, we examined by MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and intracellular reactive oxygen intermediate levels and the levels of catalase(CAT), superoxide dismutase (SOD), and glutathione peroxidase(GPX) an adaptive response of oxidative stress on B16F10 murine melanoma cell of pretreated with hydrogen peroxide. (omitted)

• Animal cells and systems
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• v.4 no.4
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• pp.341-345
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• 2000

It has been very difficult to develop and evaluate efficient fish vaccines because fish immune cells have not been properly characterized. In this study, we investigated the cell-mediated immunological properties of B- and T-like cells in Nile tilapia (Oreochromis nilotica). Surface immunoglobulin negative ($slg^{-}$) cell population proliferated in response to mammalian T-cell mitogens PHA and Con A, while surface immunoglobulin positive ($slg^{+}$) cells responded to the B-cell mitogen LPS. The slg$^{[-10]}$ cells from hemocyanin (HC)-immunized Tilapia, compared to the non-immunized control, reacted more to PHA than to Con A. Unexpectedly, antigen (Ag)-specific response was observed in both $slg^{-}$ and $slg^{-}$cells. Regardless of HC immunization, whole leukocytes from 8 head kidney of fish showed natural killer (NK)cell activity. Especially, NK cell activity was much higher in slg$^{[-10]}$ cells than in slg$^{+}$cells, indicating the possibility that fish NK cells were not at least associated with slg$^{+}$ cell population and not activated by Ag. Further understanding of functional fish immune cells will help to evaluate and develop effective vaccines for fishes and to monitor the course of therapy In infected fishes.hes.

• Journal of Acupuncture Research
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• v.18 no.1
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• pp.88-99
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• 2001

Objectives : This study was performed to determine if Orostachys japonicus A. Berger aquacupuncture (OjB) provides the protective effect against the loss of celi viability and DNA damage induced by oxidant in renal proximal tubular cells. Methods : The cell viability was evaluated by a MTT reduction assay and DNA damage was estimated by measuring double stranded DNA breaks in opossum kidney (OK) cells, an established proximal tubular cell line. Lipid peroxidation was determined by measuring malondialdehyde (MDA), a product of lipid peroxidation. Results : $H_2O_2$ increased the loss of cell viability in a time-dependent manner, which were prevented by 0.1% OjB. The protective effect of OjB was dose-dependent over concentration range of 0.05-0.5%. $H_2O_2$ caused ATP depletion and DNA damage, which were prevented by OjB and the hydrogen peroxide scavenger catalase. The loss of cell viability by $H_2O_2$ was not affected by the antioxidant DPPD, but lipid peroxidation by the oxidant was completely inhibited by DPPD. Conclusions : These data suggest that $H_2O_2$-induced death results from a lipid peroxidation-independent mechanism and the protective effect of OjB is not associated with its antioxidant activity.

• Tuberculosis and Respiratory Diseases
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• v.81 no.2
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• pp.138-147
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• 2018

Background: Recent studies show that mitophagy, the autophagy-dependent turnover of mitochondria, mediates pulmonary epithelial cell death in response to cigarette smoke extract (CSE) exposure and contributes to the development of emphysema in vivo during chronic cigarette smoke (CS) exposure, although the underlying mechanisms remain unclear. Methods: In this study, we investigated the role of mitophagy in the regulation of CSE-exposed lung bronchial epithelial cell (Beas-2B) death. We also investigated the role of a phosphodiesterase 4 inhibitor, roflumilast, in CSE-induced mitophagy-dependent cell death. Results: Our results demonstrated that CSE induces mitophagy in Beas-2B cells through mitochondrial dysfunction and increased the expression levels of the mitophagy regulator protein, PTEN-induced putative kinase-1 (PINK1), and the mitochondrial fission protein, dynamin-1-like protein (DRP1). CSE-induced epithelial cell death was significantly increased in Beas-2B cells exposed to CSE but was decreased by small interfering RNA-dependent knockdown of DRP1. Treatment with roflumilast in Beas-2B cells inhibited CSE-induced mitochondrial dysfunction and mitophagy by inhibiting the expression of phospho-DRP1 and -PINK1. Roflumilast protected against cell death and increased cell viability, as determined by the lactate dehydrogenase release test and the MTT assay, respectively, in Beas-2B cells exposed to CSE. Conclusion: These findings suggest that roflumilast plays a protective role in CS-induced mitophagy-dependent cell death.

• Archives of Pharmacal Research
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• v.16 no.4
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• pp.259-264
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• 1993

Three cell lines, CHO, L929 and B16 which are non-tumorigenic and cancer cells, respectively, were first tested for their survival in the presence of radioprotective ginseng protein fraction(GPF0. The influence of three radioprotectors-CPF, cysteamine, and 1-Methyl-2-bis[(2-methylthio)vinyl] quinolinium iodide (MVQI) on DNA repair capacity of UV damaged cells survival test, the GPF showed higher cytotoxicity in L929 and B16 than in CHO cells. However, the degree of cell killing was also investigated by measuring $^3H$-thymidine incorporation of PUVA treated cells. In cell survival test, the GPF showed higher cytotoxicity in L929 and B16 than in CHO cells. However, the degree of cell killing was not high enough to consider it as an antitumorigenic agent. Variable results were obtained in the effects on DNA repair capacity depending on the protectors and cell lines used. In pretreatment, the presence of GPF and MVOI brought about a sinificant increase in the capacity in both CHO and B16 cells. However, in L929, the enhancing effect was not shown. In all three cell lines, cysteamine showed lower repair capacity than control, suggesting the primary damage reduction in stronger enhancing effects in L929 and B16 cells, while it was weaker in CHO cells. Here also cystemine hsowed a very little or no increase in the capacity in all three cell lines. These results demonstrate that GPF has mild cytotoxicity in tumorignic cells and that GPF and MVQI enhance DNA repair capacity of UV damaged cells, whether they are tumorigenic or not. On the other hand, cysteamine shows only damage reduction effect. Celles of different genetic origin seem to give different responses to the modifier and different modifiers may possibly work by different mechanisms.

• Applied Biological Chemistry
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• v.38 no.4
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• pp.308-312
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• 1995

The effects of nitrogen, phosphate in modified B5 medium and cell immobilization on cell growth and taxol production were investigated using cell cultures of Taxus cuspidata. The ratio of nitrate to ammonium was found to be an important parameter. The ratio of 1 increased taxol production 10-fold, compared to the original ratio of 20 in modified B5 medium. Reducing phosphate concentration inhibited cell growth, but increased taxol production noticeably. Immobilized cells produced a taxol concentration of ${\sim}120\;g/l$

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.4
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• pp.1517-1520
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• 2014

Aim: To investigate effects of sulforaphane on the BIU87 cell line and underlying mechanisms involving IGFBP-3. Methods: Both BIU87 and IGFBP-3-silenced BIU87 cells were treated with sulforaphane. Cell proliferation was detected by MTT assay. Cell cycle and apoptosis were determined via flow cytometry. Quantitative polymerase chain reaction and Western blotting were applied to analyze the expression of IGFBP-3 and NF-${\kappa}B$ at both mRNA and protein levels. Results: Sulforaphane (80 ${\mu}M$) treatment could inhibit cell proliferation, inducing apoptosis and cell cycle arrest at G2/M phase. All these effects could be antagonized by IGFBP-3 silencing. Furthermore, sulforaphane (80 ${\mu}M$) could down-regulate NF-${\kappa}B$ expression while elevating that of IGFBP-3. Conclusions: Sulforaphane could suppress the proliferation of BIU87 cells via enhancing IGFBP-3 expression, which negatively regulating the NF-${\kappa}B$ signaling pathway.