• Asian Pacific Journal of Cancer Prevention
• /
• v.16 no.2
• /
• pp.761-767
• /
• 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.

• BMB Reports
• /
• v.35 no.1
• /
• pp.94-105
• /
• 2002

Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to actively participate in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents that target this cell death process. This review will focus on molecular cell death pathways that are responsible for generating the apoptotic phenotype. It will also summarize what is currently known about the apoptotic signals that are activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2003.05a
• /
• pp.68-69
• /
• 2003

Tributyltin (TBT) used world-wide in antifouling paints for ships is a widespread environmental pollutant and cause reproductive organs atrophy in rodents. At low doses, antiproliferative modes of action have been shown to be involved, whereas at higher doses apoptosis seems to be the mechanism of toxicity in reproductive organs by TBT. (omitted)

• Asian Pacific Journal of Cancer Prevention
• /
• v.13 no.10
• /
• pp.4873-4878
• /
• 2012

Apoptosis is programmed cell death which is essential for development and survival of living organisms. It is a sequentially regulated suicidal programme where cells activate certain enzymes which dissolute their own nuclear component and various protein component of nucleus and cytoplasm. Disturbance of this regulatory pathway may lead to various diseases like autoimmune diseases, neurodegenerative diseases and cancers. The potential mechanisms of apoptosis and its role in cancer are discussed. The ability of apoptosis to modulate the life or death of a cell is also recognized for its immense therapeutic potential. Understanding the mechanisms from this review will give us better insight to the pathogenesis of various diseases including cancer and will open new horizons to therapeutic approaches.

• Asian Pacific Journal of Cancer Prevention
• /
• v.14 no.2
• /
• pp.891-894
• /
• 2013

The present study was performed to assess the activity of the botulinum toxin A on breast cancer cells. The T47D cell line was exposed to diverse concentrations of the botulinum toxin A and cell viability and apoptosis were estimated using MTT and propidium iodine/annexin V methods, respectively. Botulinum toxin A exerted greater cytotoxic activity in T47D cells in comparison with MCF10A normal cells; this appeared to be via apoptotic processes caspase-3 and -7. In conclusion, botulinum toxin A induces caspase-3 and -7 dependent apoptotic processes in the T47D breast cancer cell line.

• Toxicological Research
• /
• v.29 no.4
• /
• pp.257-261
• /
• 2013

${\alpha}$-Curcumene is one of the physiologically active components of Curcuma zedoaria, which is believed to perform anti-tumor activities, the mechanisms of which are poorly understood. In the present study, we investigated the mechanism of the apoptotic effect of ${\alpha}$-curcumene on the growth of human overian cancer, SiHa cells. Upon treatment with ${\alpha}$-curcumene, cell viability of SiHa cells was inhibited > 73% for 48 h incubation. ${\alpha}$-Curcumene treatment showed a characteristic nucleosomal DNA fragmentation pattern and the percentage of sub-diploid cells was increased in a concentration-dependent manner, hallmark features of apoptosis. Mitochondrial cytochrome c activation and an in vitro caspase-3 activity assay demonstrated that the activation of caspases accompanies the apoptotic effect of ${\alpha}$-curcumene, which mediates cell death. These results suggest that the apoptotic effect of ${\alpha}$-curcumene on SiHa cells may converge caspase-3 activation through the release of mitochondrial cytochrome c.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.19 no.5
• /
• pp.1363-1369
• /
• 2005

Previously we have shown that shikonin has strong anti-tumor activities via inducing apoptosis and suppressing metastasis on LLC cells in vivo and in vitro. Here we have investigated anti-angiogenic potential of shikonin and its possible mechanism of action in HSE cells. Shikonin inhibited the proliferation of HSE cells in a concentration-dependent manner. It was shown that this proliferation inhibition was caused by apoptosis induced by shikonin via BrdU incorporation and Western blotting analysis. Shikonin treatment was caused that decrease of activation of caspases and cleavage of PARP. And shikonin induced that the activation of mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38. Moreover, shikonin showed anti-angiogenic activities inhibiting tube-like formation of HSE cells in vitro and vascular formation of LLC cells in vivo. These findings suggest that shikonin may a possible candidate not only anti-metastatic agent but also anti-angiogenic agent.

• Biomolecules & Therapeutics
• /
• v.20 no.1
• /
• pp.62-67
• /
• 2012

TNF-related apoptosis-inducing ligand (TRAIL) is a promising agent for management of cancer because of its selective cytotoxicity to cancer cells. However, some cancer cells have resistance to TRAIL. Accordingly, novel treatment strategies are required to overcome TRAIL resistance. Here, we examined the synergistic apoptotic effect of apigenin in combination with TRAIL in Huh-7 cells. We found that combined treatment of TRAIL and apigenin markedly inhibited Huh-7 cell growth compared to either agent alone by inducing apoptosis. Combined treatment with apigenin and TRAIL induced chromatin condensation and the cleavage of poly (ADP-ribose) polymerase (PARP). In addition, enhanced apoptosis by TRAIL/apigenin combination was quantified by annexin V/PI flow cytometry analysis. Western blot analysis suggested that apigenin sensitizes cells to TRAIL-induced apoptosis by activating both intrinsic and extrinsic apoptotic pathway-related caspases. The augmented apoptotic effect by TRAIL/apigenin combination was accompanied by triggering mitochondria-dependent signaling pathway, as indicated by Bax/Bcl-2 ratio up-regulation. Our results demonstrate that combination of TRAIL and apigenin facilitates apoptosis in Huh-7 cells.

• YAKHAK HOEJI
• /
• v.56 no.1
• /
• pp.35-41
• /
• 2012

In this study, we examined the effect of luteolin to enhance TRAIL-induced anticancer effect in SK-Hep1 cells. We found that combined use of TRAIL with luteolin markedly enhanced the cytotoxicity compared to either agent alone by inducing apoptosis. Furthermore, combined treatment of TRAIL with luteolin significantly induced activation of death receptor pathway-related proteins as well as PARP-cleavage and activation of effector caspases. Also, our result indicated that upregulation of DR4 and DR5 by luteolin combination may contribute to enhanced susceptibility of SK-Hep1 cells to TRAIL.

• Animal cells and systems
• /
• v.9 no.4
• /
• pp.181-190
• /
• 2005

BIRPs (BIR containing Proteins) which contain one to three BIR domains constitute a highly conserved family from yeast to human. BIR domains mediate the interaction of BIRPs with various other proteins. Some of the members acquire a Ring domain which acts as an E3 ubiquitin ligase. The first member of BIRPs identified in the baculovirus was found as an inhibitor of apoptosis and most of the family members in the other species have been recognized to have the same function which bind to and inhibit caspases, thereby suppresses apoptotic cell death. But an increasing number of evidences indicate that BIRPs are involved in various cellular events such as cell division, control of cell cycle, signal transduction, cell migration, innate immunity as well as regulation of apoptosis. In this review, we summarize the structural and functional features of the BIRPs, especially focus on the various functions of BIRPs unrelated to regulation of apoptosis by the recent findings.