• IMMUNE NETWORK
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• v.6 no.2
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• pp.59-66
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• 2006

Background: CM1 (Centrocyte/-blast Marker I) defined by a mAb developed against concanavalin-A activated PBMC, is expressed specifically on a subpopulation of centroblasts and centrocytes of human germinal center (GC) B cells. Burkitt lymphoma (BL) is a tumor consisting of tumor cells with the characteristics of GC B cell. Previously we reported that CM1 ligation with anti-CM1 mAb induced apoptosis in Ramos $(IgM^{high})$ and Raji $(IgM^{low})$ cells. Methods & Results: In the present study, we observed that CM1 ligation with anti-CM1 mAb induced Fas ligand and Fas expression in Ramos cells, but not in Raji cells. Furthermore, anti-Fas blocking antibody, ZB4, blocked CM1-mediated apoptosis effectively in Ramos cells, but not in Raji cells. Increased mitochondrial membrane permeabilization, which was measured by $DiOC_6$, was observed only in Raji cells. In contrast to no significant change of Bax known as pro-apoptotic protein, anti-apoptotic protein Bcl-2 was significantly decreased in Raji cells. In addition, we observed that CM1 ligation increased release of mitochondrial cytochrome c and upregulated caspase-9 activity in Raji cells. Conclusion: These results suggest that apoptosis induced by CM1-ligation is mediated by Fas-Fas ligand interaction in Ramos cells, whereas apoptosis is mediated by down-regulation of Bcl-2 and subsequent decrease of mitochondrial membrane potential in Raji cells.

• Natural Product Sciences
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• v.6 no.3
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• pp.147-150
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• 2000

The extracts of Carica papaya (flower), Barringtonia macrostachya (leaves), Coleus tuberosus (tuber), Mangifera indica (fruit skin) and Eugenia polyantha (leaves) showed strong in vitro anti-tumor promoting activity when assayed using Raji cells (Mooi et al., 1999). The antitumor promoting activity of the crude extracts was further analyzed by immunoblotting analysis of Raji cells carving Epstein-Barr virus genome. The expression of early antigens diffuse (EA-D) and early antigens restricted (EA-R) was determined by performing western blotting of treated Raji cells with human sera of nasopharyngeal carcinoma patients. All the plant extracts were shown to be able to suppress both EA-D and EA-R.

• Advances in Traditional Medicine
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• v.3 no.3
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• pp.151-156
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• 2003

The leaves of Mirabilis jalapa L contains protein fraction presumed ribosome-inactivating protein (RIP). RIP is a group of protein that has RNA N-glycosidase activity that is capable to inhibit protein synthesis. Protein fraction of the plant was shown to be cytotoxic on HeLa cell-line, however, the mechanism by which the protein kill the cells is not identified yet, whether trough apoptosis, necrosis, or other mechanism. This research aim to study the mechanism of cell death caused by the protein fraction isolated from the leaves of this plant on HeLa and Raji cell-line, as representative of different kind of cancer cells. Results showed that protein fraction isolated from the leaves of Mirabilis jalapa L was more cytotoxic to HeLa cell-line (LC50: 0.65 mg/ml) than to Raji cell-line (1.815 mg/ml) on 48 hours incubation time. Moreover, it was demonstrated that the death of HeLa cells caused by the protein fraction was due to induction of apoptosis, while on Raji cell-line was due to non-apoptosis way, presumably via necrosis.

• The Journal of Internal Korean Medicine
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• v.12 no.2
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• pp.1-15
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• 1991

Bigihwan which has been widely used in Oh-jug in oriental Medicine was investigated on its antitumor effect employing blood cancer cell lines. K 562 derived from human erytholeukemia, Raji from lymphoma and $MO_4$ from hlastogenic cancer were used in this study to see the analytical evaluation of Bigihwan' s antitumor effect using three different kinds of methods such as $^{3}H-thymidine$ up take assay. MTT assay and live cell counts by Trypan blue assay. The result obtained are as follows. 1. When higher than 10% Bigihwan was treated. inhibitory effect of tumor killing action was observed showing the increasing order of $MO_4$, K 562 and Raji(Fig. 3). 2. When 1 to 5% of Bigi-hwan was treated, 4 to 30% of tumor cell survival was observed according to various blood tumor cell lines suggesting that antitumor effect of Bigi-hwan was different as the characteristics of tumor cells showing 70 to 95% cell killing effent(Fig. 4). 3. Compared the survivals of cells by relative scales though the initial cpm was variable because of different cell growth rate. Raji was most effective being killed 95% by the treatment of 1% Bigihwan while Raji and K562 showed 93% by 5% Bigihwan.(Fig. 5) 4. The survival rate of Raji derived from Burkitt lymphoma was rather increased to 2.3 times when Bigihwan concentration was increased from 1 to 10% lmplying of refraining from over use of this anticancer drug. specially to lymphoma patients(Fig. 5). 5. Bigihwan was most effective to K 562 and then $MO_4$ showing 95% tumor cell death by using 1% of this anticancer drug while it was least effective to Raji showing only 68% of tumor cell death(Fig.7). 6. Judging from the all the analytical methods used in this study, through all different three tumor cell lines. Bigihwan was most effective to K 562 derived from human erythroleukemia.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1177-1182
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• 2012

Protein kinase C (PKC) has been implicated in carcinogenesis and displays variable expression profiles during cancer progression. Studies of dietary phytochemicals on cancer signalling pathway regulation have been conducted to search for potent signalling regulatory agents. The present study was designed to evaluate any suppressive effect of maslinic acid on PKC expression in human B-lymphoblastoid cells (Raji cells), and to identify the PKC isoforms expressed. Effects of maslinic acid on PKC activity were determined using a PepTag$^{(R)}$ assay for non-radioactive detection of PKC. The highest expression in Raji cells was obtained at 20 nM PMA induced for 6 hours. Suppressive effects of maslinic acid were compared with those of four PKC inhibitors (H-7, rottlerin, sphingosine, staurosporine) and two triterpenes (oleanolic acid and ursolic acid). The $IC_{50}$ values achieved for maslinic acid, staurosporine, H-7, sphingosine, rottlerin, ursolic acid and oleanolic acid were 11.52, 0.011, 0.767, 2.45, 5.46, 27.93 and $39.29\;{\mu}M$, respectively. Four PKC isoforms, PKC ${\beta}I$, ${\beta}II$, ${\delta}$, and ${\zeta}$, were identified in Raji cells via western blotting. Maslinic acid suppressed the expression of PKC ${\beta}I$, ${\delta}$, and ${\zeta}$ in a concentration-dependent manner. These preliminary results suggest promising suppressive effects of maslinic acid on PKC activity in Raji cells. Maslinic acid could be a potent cancer chemopreventive agent that may be involved in regulating many downstream signalling pathways that are activated through PKC receptors.

• Natural Product Sciences
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• v.5 no.1
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• pp.33-38
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• 1999

Ethanolic extracts of different parts of 10 local traditional vegetables (ulam) (Amaranthus gangeticus, Jussiaea linifolia, Eugenia polyantha, Trapa incisa, Trichosanthes anquina, Mangifera indica, Pachyrrhirus erosus, Barringtonia mcarostachya, Carica papaya, and Coleus tuberosus) were screened for in vitro antitumor promoting activity using the inhibition test of Epstein-Barr virus (EBV) activation in Raji cells induced by phorbol 12-myristate 13-acetate and sodium-n-butyrate. All the extracts were found to have strong inhibition activity toward EBV-activation, except for leaf extract of T. anquina. The extracts were non-cytotoxic to the Raji cells except for the extracts of A. gangeticus (leaves), B. macrostachya (leaves), E. polyantha (young leaves), and J. linifolia (leaves) where the viability of the cells were decreased significantly.

• Molecules and Cells
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• v.27 no.3
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• pp.283-289
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• 2009

Curcumin, a natural compound extracted from rhizomes of curcuma Curcuma species, has been shown to possess potent anti-inflammatory, anti-tumor and anti-oxidative properties. However, the mechanism of action of the compound remains poorly understood. In this report, we have analyzed the effects of curcumin on the cell proliferation of Burkitt's lymphoma Raji cells. The results demonstrated that curcumin could effectively inhibit the growth of Raji cells in a dose- and time-dependent manner. Further studies indicated that curcumin treatment resulted in apoptosis of cells. Biochemical analysis showed that the expression of Bax, Bid and cytochrome C were up-regulated, while the expression of oncogene c-Myc was down regulated after curcumin treatment. Furthermore, poly (ADP-ribose) polymerase (PARP) cleavage was induced by the compound. Interestingly, the antiapoptotic Bcl-2 expression was not significantly changed in Raji cells after curcumin treatment. These results suggested that the mechanism of action of curcumin was to induce mitochondrial damage and therefore led to Raji cell apoptosis. We further investigated the in vivo effects of curcumin on the growth of xenograft tumors in nude mice. The results showed that curcumin could effectively inhibit tumor growth in the xenograft mouse model. The overall results showed that curcumin could suppress the growth of Burkitt's lymphoma cells in both in vitro and in vivo systems.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.6
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• pp.345-349
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• 2004

Heat shock ($43^{\circ}C$ for 60 minutes) is sufficient to induce apoptosis in a wide number of cell lines. In this study, we asked whether DNA strand breaks are responsible for this phenomenon. Using the highly sensitive comet assay for DNA damage detection, we were unable to demonstrate DNA breaks immediately after heat shock in Raji human Iymphoid cells. It showed that DNA breaks were not necessary for hyperthermic apoptosis, since its activity is indicative of DNA lesions. Here, we present a suggestion that a protein(s) is the major target for heat shock apoptosis. We firstly found glycerol, which reportedly stabilizes protein structure, showed a protective effect in Raji cells against hyperthermic apoptosis. In addition, quercetin, which modulates transcription of the heat shock protein family members, enhanced apoptotic death induced by hyperthermia. Furthermore, Raji cells are protected by a pre-mild heat treatment prior to the killing dose of heat shock.

• BMB Reports
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• v.49 no.10
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• pp.560-565
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• 2016

Granzyme A (GzmA) was first identified as a cytotoxic T lymphocyte protease protein with limited tissue expression. A number of cellular proteins are known to be cleaved by GzmA, and its function is to induce apoptosis. Histones H1, H2B, and H3 were identified as GzmA substrates during apoptotic cell death. Here, we demonstrated that histone H4 was cleaved by GzmA during staurosporine-induced cell death; however, in the presence of caspase inhibitors, staurosporine-treated Raji cells underwent necroptosis instead of apoptosis. Furthermore, histone H4 cleavage was blocked by the GzmA inhibitor nafamostat mesylate and by GzmA knockdown using siRNA. These results suggest that histone H4 is a novel substrate for GzmA in staurosporine-induced cells.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.14
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• pp.5715-5719
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• 2014

Autophagy is crucial in the maintenance of homeostasis and regenerated energy of mammalian cells. Macroautophagy and chaperone-mediated autophagy(CMA) are the two best-identified pathways. Recent research has found that in normal cells, decline of macroautophagy is appropriately parallel with activation of CMA. However, whether it is also true in cancer cells has been poorly studied. Here we focused on cross-talk and conversion between macroautophagy and CMA in cultured Burkitt lymphoma Raji cells when facing serum deprivation and exposure to a toxic compound, arsenic trioxide. The results showed that both macroautophagy and CMA were activated sequentially instead of simultaneously in starvation-induced Raji cells, and macroautophagy was quickly activated and peaked during the first hours of nutrition deprivation, and then gradually decreased to near baseline. With nutrient deprivation persisted, CMA progressively increased along with the decline of macroautophagy. On the other hand, in arsenic trioxide-treated Raji cells, macroautophagy activity was also significantly increased, but CMA activity was not rapidly enhanced until macroautophagy was inhibited by 3-methyladenine, an inhibitor. Together, we conclude that cancer cells exhibit differential responses to diverse stressor-induced damage by autophagy. The sequential switch of the first-aider macroautophagy to the homeostasis-stabilizer CMA, whether active or passive, might be conducive to the adaption of cancer cells to miscellaneous intracellular or extracellular stressors. These findings must be helpful to understand the characteristics, compensatory mechanisms and answer modes of different autophagic pathways in cancer cells, which might be very important and promising to the development of potential targeting interventions for cancer therapies via regulation of autophagic pathways.