• BMB Reports
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• 제29권3호
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• pp.200-204
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• 1996

Nerve growth factor (NGF) is literally known to promote neural differentiation and survival in several peripheral and central neurons. Thus, it is Widely believed that NGF may serve as a therapeutic agent for many types of neuronal diseases. One of the mechanisms suggested to explain the protective role of NGF is that the trophic factor can prevent the increase of intracellular calcium ions which might be responsible for neural death. To examine whether or not the calcium hypothesis works even under pathological conditions, we applied NGF to cultures deprived of glucose. Surprisingly, what was observed here is that NGF rather promoted cell death under a glucose-deprived condition. What we call the NGF paradox phenomenon occurred in a calcium concentration-dependent manner, indirectly suggesting that NGF might increase intracellular calcium ions in cells deprived of glucose. This suggestion is further supported by the fact that nifedipine, a well-known L-type calcium channel blocker, could block the cell death potentiated by NGF. Here it is still premature to propose the complete mechanism underlying the NGF paradox phenomenon. However, this study certainly indicates that NGF as a therapeutic agent for neuronal diseases should be carefully considered before use.

• Animal cells and systems
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• 제15권1호
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• pp.1-8
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• 2011

Perturbation of metabolism with increased expression of lipogenic enzymes is a common characteristic of human cancers, including prostate cancer. In the present work the overexpression of stearoyl-CoA desaturase (SCD) in LNCaP cells led to increased mRNA levels of fatty acid synthase (FAS) and acetyl-CoA-carboxylase-a, whereas micro RNA-mediated silencing of SCD inhibited the expression of these lipogenic genes in LNCaP cells. Treatment with the FAS-specific inhibitor cerulenin inhibited SCD induction of LNCaP cell proliferation. In addition, a transient transfection assay revealed the capability of cerulenin to suppress SCD and dihydrotestosterone induction of androgen receptor transcriptional activity. Furthermore, overexpression of SCD in LNCaP cells produced marked resistance to ceramide-induced cell death with reduced poly(ADP-ribose) polymerase (PARP) cleavage. In contrast, silencing of SCD expression increased Bax protein in LNCaP cells. Furthermore, addition of ceramide to SCD knockdown LNCaP cells increased cell death and caspase-3 activity with drastic increase of PARP cleavage. Together, the data indicate that SCD may provide resistance of prostate cancer cells to ceramide-induced cell death.

• 한국동물학회:학술대회논문집
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• 한국동물학회 1997년도 한국생물과학협회 학술발표대회
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• pp.192.1-192
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• 1997

No Abstract, See Full Text

• Asian Pacific Journal of Cancer Prevention
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• 제16권2호
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• pp.761-767
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• 2015

Background: In this study, we used Daucus carota oil extract (DCOE) to target acute myeloid leukemia (AML) cells. All the AML cell lines tested were sensitive to the extract while peripheral mononuclear cells were not. Analysis of mechanism of cell death showed an increase in cells positive for annexinV and for active caspases, indicating that DCOE induces apoptotic cell death in AML. Inhibition of the MAPK pathway decreased sensitivity of AML cells to DCOE, indicating that cytotoxicity may be dependent on its activity. In conclusion, DCOE induces selective apoptosis in AML cells, possibly through a MAPK-dependent mechanism.

• 대한약침학회지
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• 제25권4호
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• pp.390-395
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• 2022

Objectives: Sweet bee venom (sBV) is purified from Apis mellifera, containing a high level of melittin-its main component. It has been used as a therapeutic agent for pain relief and anti-inflammation, as well as for treating neuronal abnormalities. Recently, there have been studies on the therapeutic application of sBV for anticancer treatment. In the present study, we investigated the pharmacological effect of sBV treatment in A549 human lung cancer cells. Methods: We used microscopic analysis to observe the morphological changes in A549 cells after sBV treatment. The MTT assay was used to examine the cytotoxic effect after dose-dependent sBV treatment. Molecular changes in sBV were evaluated by the expression of apoptosis marker proteins using western blot analysis. Results: Microscopic analysis suggested that the growth inhibitory effect occurred in a dose-dependent manner; however, cell lysis occurred at a concentration over 20 ㎍/mL of sBV. The MTT assay indicated that sBV treatment exhibited a growth inhibitory effect at a concentration over 5 ㎍/mL. On fluorescence activated cell sorting analysis, G0 dead cells were observed after G1 arrest at treatment concentrations up to 10 ㎍/mL. However, rapid cell rupture was observed at a concentration of 20 ㎍/mL. Western blot analysis demonstrated that sBV treatment modulated the expression of multiple cell death-related proteins, including cleaved-PARP, cleaved-caspase 9, p53, Bcl2, and Bax. Conclusion: sBV induced cell death in A549 human lung cancer cells at a pharmacological concentration, albeit causing hemolytic cell death at a high concentration.

• 대한수사과학회지
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• 제1권2호
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• pp.44-56
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• 2006

The reform necessity of medicolegal death investigation system is continuously issued. The problems from the current death investigation system are discussed, specially on the professionalism of the involved personnel such as policemen, doctors, prosecutors. Death investigation exists not only to prosecute the criminals but also primarily to protect the general public's health, safety, and welfare. The reform proposals of death investigation system are followed as below. Statutes require that the prosecutor be notified of certain deaths. All deaths that may reasonably result from anything other than natural disease should be investigated. A death certificate is a legal document which authenticate a death, therefore it is issued by the doctor. The postmortem examination must be rearranged on the university base and performed by the qualified doctors who are trained at least in pathology. The police officer specified in death investigation and forensic identification should be encouraged to keep doing their special work in many ways.

• International Journal of Oral Biology
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• 제31권3호
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• pp.81-86
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• 2006

SET (Suppressor of variegation, Enhancer of zeste, and the Trithorax) domain-containing proteins are known to have methyltransferase activity at lysine residues of histone proteins. In this study, we identified a novel SET domain-containing protein from mouse and named Kodo7. Indeed, Kodo7 has methyltransferase activity at K9 residue of the H3 protein as demonstrated by a histone methyl-transferse activity assay using GST-tagged Kodo7. Confocal microscopy showed that Kodo7 is co-localized with histones in the nucleus. Interestingly, ectopic expression of Kodo7 by transient transfection induced cell death and treatment of the transfectants with a caspase-3 inhibitor, Ac-DEVD-AFC decreased Kodo7-induced apoptosis. These results suggest that Kodo7 induces apoptotic cell death through increased methylation of histones leading to transcriptional repression.

• BMB Reports
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• 제48권5호
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• pp.289-294
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• 2015

Caesalpinia sappan is a well-distributed plant that is cultivated in Southeast Asia, Africa, and the Americas. C. sappan has been used in Asian folk medicine and its extract has been shown to have pharmacological effects. Two homoisoflavonoids, sappanol and brazilin, were isolated from C. sappan by using centrifugal partition chromatography (CPC), and tested for protective effects against retinal cell death. The isolated homoisoflavonoids produced approximately 20-fold inhibition of N-retinylidene-N-retinyl-ethanolamine (A2E) photooxidation in a dose-dependent manner. Of the 2 compounds, brazilin showed better inhibition (197.93 ± 1.59 μM of IC₅₀). Cell viability tests and PI/Hoechst 33342 double staining method indicated that compared to the negative control, sappanol significantly attenuated H₂O₂-induced retinal death. The compounds significantly blunted the up-regulation of intracellular reactive oxygen species (ROS), and sappanol inhibited lipid peroxidation in a concentration-dependent manner. Thus, both compounds represent potential antioxidant treatments for retinal diseases. [BMB Reports 2015; 48(5): 289-294]

• Preventive Nutrition and Food Science
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• 제7권2호
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• pp.128-132
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• 2002

The present study was performed to observe the role of protein kinase C (PKC) inhibitors (H-7, staurosporine) and daunorubicin in the cell death process of MCF7 cells; and examined whether or not the type of induced cell death was apoptosis. The usefulness of the combined therapy of PKC inhibitors and daunorubicin to improve the adverse effect of daunorubicin was also investigated. Cell death was induced by treatment with PKC inhibitors or daunorubicin. Characteristic morphologic features of cell shrinkage, chromatic condensation, and cytoplasmic vacuolization were observed. These treatments also stimulated the cleavage of poly-(ADP-ribose) polymerase (PARP), an early event in apoptosis. With slight differences in the percentage of apoptosis-induced cells, staurosporine, H-7 and daunorubicin effectively induced apoptosis in MCF7 cells. Furthermore, combined treatment of PKC inhibitors and daunorubicin significantly drove the cells into an apoptotic state. Hence, our results revealed the possible therapeutic value of combined therapy for the prevention of drug resistance and adverse side effects.

• 대한의생명과학회지
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• 제29권3호
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• pp.178-183
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• 2023

Natural killer (NK) cells are innate cytotoxic lymphoid cells that actively prevent neoplastic development, growth, and metastatic dissemination in a process called cancer immunosurveillance. Regulation of the cytotoxic activity of NK cells relies on integrated interactions between inhibitory receptors and numerous activating receptors that act in tandem to eliminate tumor cells efficiently. Conventional chemotherapy is designed to produce an anti-proliferative or cytotoxic effect on early tumor cell division. Therapies designed to kill cancer cells and simultaneously maintain host anti-tumor immunity are attractive strategies for controlling tumor growth. Depending on the drug and dose used, several chemotherapeutic agents cause DNA damage and cancer cell death through apoptosis, immunogenic cell death, or other forms of non-killing (i.e., mitotic catastrophe, senescence, autophagy). Among stress-induced immunostimulatory proteins, changes in the expression levels of NK cell activating and inhibitory ligands and tumor cell death receptors play an important role in the detection and elimination by innate immune effectors including NK cells. Therefore, we will address how these cytotoxic lymphocytes sense and respond to high and low concentrations of drug-induced stress to the drug cisplatin, among the various types of drugs that contribute to their anticancer activity.