Classical dihydropyrrole[3,4-f]quinazoline antifolates 7,8 and 9, in which the tricyclic ring is structurally similar to the pteridine ring of $CH_2-THF(1)$, the cofactor of thymidylate synthase (TS), were synthesized, and their in vitro antitumor activity was evaluated by measuring the cell growth inhibitory activity against cancer cell lines. The target compounds were cytotoxic against CCRF-CEM, human T-cell acute lymphoblastic leukemia, with the cell growth inhibitory activity $(IC_{50})$ of $0.8{\sim}8.3\;{\mu}M$. Among the three compounds, 3-amino analog 7 was 10- and 3.5-fold more cytotoxic compared to the 3-methyl analogs 8 and 9, and its cytotoxicity was similar to that of the reference compound with the $IC_{50}$ value of $0.83\;{\mu}M$. This result was supposed as the consequence of the fact that dihydropyrroloquinazolinone ring with amino group was able to bind well in the active site of TS. In the case of 3-methyl analogs, analog 9, which has two-carbon bridge between the dihydropyrroloquinazolinone ring and benzoyl-L-glutamic acid, was 3-times more potent in cytotoxicity than analog 8 which has one-carbon bridge, and this result indicates that the distance and conformational orientation of the benzoyl-L-glutamic acid moiety with respect to the tricyclic ring may also be a crucial determinant of cell growth inhibitory activity.
Park, Youn-Hee;Chun, En-Mi;Bae, Myung-Ae;Seu, Young-Bae;Song, Kyung-Sik;Kim, Young-Ho
Journal of Microbiology and Biotechnology
/
v.10
no.1
/
pp.27-34
/
2000
The chloroform and methanol (2;1, v/v) extract from an edible plant, Actinidia arguta Planchon, appeared to possess antitumor activity against human leukemias Jurkat T and U937 cells through inducing apoptosis. The substance in the solvent extract was purified by silica gel column chromatography, preparative TLC, and Sephadex LH-20 column chromatography. Characteristics of the substance analyzed by UV scanning analysis, $^1H$ and $^{13}C$ NMR spectra suggested that the substance belongs to the chlorophyll derivatives-like group. The $IC_{50}$ value of the chlorophyll derivative (Cp-D) determined by MTT assay was $15\mu\textrm{g}/ml$ for Jurkat, $10\mu\textrm{g}/ml$ for U937, and $11.4\mu\textrm{g}/ml$ for HL-60m and was more toxic to these leukemias than to solid tumors or normal fibroblast. In order to elucidate cellular mechanisms underlying the cytotoxicity, the effect of the Cp-D on Jurkat T cells was investigated. When cells were treated with the Cp-D at a concentration of $15\mu\textrm{g}/ml$, [3H]thymidine incorporation declined rapidly and wa undetectable in 1h. However, no significant changes were made in the cell cycle distribution of the cells by 24h. The sub-Gl peak representing apoptotic cells began to be detectable in 36h, at which time apoptotic DNA fragmentation was also detected on agarose gel electrophoresis, demonstrating that the cytotoxic effect of the Cp-D is attributable to the induced apoptosis. Under the same conditions, although the protein level of cyclin-dependent kinases such as cdc4, csk6, cdk2, and cdc2 was not significantly changed until 24h, the kinase activity of all c안 rapidly declined and reached a minimum level within 1-6h and then recovered to the initial level by 12h and sustained until 24h. These results suggest that inactivation of cdks at an inappropriate time during the cell cycle progression in jurkat T cells following a treatment with the Cp-D leads to induction of apoptotic cell death.
Kim Tae Hwan;Kim Sung Ho;Chung In Yong;Cho Chul Koo;Ko Kyung Hwan;Yoo Seong Yul
Radiation Oncology Journal
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v.11
no.2
/
pp.219-225
/
1993
The evaluation of radiation-induced DNA double strand breaks (DSB) was made following irradiation of human lymphocytes, murine lymphocytes and EL-4 leukemia cells over a wide dose range of $^{60}Co\;{gamma}-rays.$ In lipopolysaccharide (LPS) or phytohemagglutinin (PHA)-stimulated murine lymphocytes, the slopes of the stand scission factor (SSF) revealed that lymphocytes with LPS increased DNA DSB formation by a factor of 1.432 (p<0.005). Furthermore, strand break production was relatively inefficient in the T lymphocytes compared to the B lymuhocytes. And EL-4 leukemia cells were found to form significantly more DNA DSB to a greater extent than normal lymphocytes (p<0.005). The in vitro studies of the intrinsic radiosensitivity between human lymphocytes and murine lymphocytes showed similar phasic kinetics. However, murine lymphocytes were lower in DNA DSB formation and higher in the relative radiation dose of 10 percent DNA strand breaks at 3.5 hours following ${gamma}-irradiation$ than human lymphocytes. Though it is difficult to interpret these results, these differences may be result from environmental and genetic factors. From our data, if complementary explanations for this difference will be proposed, the differences in the dose-effect relationship for the induction of DSB between humans and mice must be related to interspecies variations in the physiological condition of the peripheral blood in vitro and not to differences in the intrinsic radiation sensitivity of the lymphocytes. These results can be estimated on the basis of dose-effect correlation enabling the interpretation of clinical response and the radiobiological parameters of cytometrical assessment.
In a previous paper (Kim et al., 1996a), the immediate 5' -flanking region and coding region of the human UDP-N -acetylglucosamine:-D-mannoside-1,4-Nacetylglucosaminyltransferase III (N-acetylglucosaminyitransferase- III; GnT-III) gene was reported, isolated and analyzed. Herein, we report on amplification of a new 5' -noncoding region of the GnT-III mRNA by single-strand ligation to single-stranded cDNA-PCR (5' -RACE PCR) using poly(A)+ RNA isolated from human fetal liver cells. A cDNA clone was obtained with 5' sequences (96 bp) that diverged seven nucleotides upstream from the ATG (+1) start codon. A concensus splice junction sequence, TCTCCCGCAG, was found immediately 5' to the position where the sequences of the cDNA diverged. The result suggested the presence of an intron in the 5' -noncoding region and that the cDNA was an incompletely reversetranscribed cDNA product derived from an mRNA containing a new noncoding exon. When mRNA expression of GnT-III in various human tissues and cancer cell lines was examined, Northern blot analysis indicated high expression levels of GnT-III in human fetal kidney and brain tissues, as well as for a number of leukemia and lymphoma cancer cell lines. Promoter activities of the 5' -flanking regions of exon 1 and the new noncoding region were measured in a human hepatoma cell line, HepG2, by luciferase assays. The 5'-flanking region of exon 1 was the most active, whilst that of exon 2 was inactive.
Proceedings of the Korean Society of Developmental Biology Conference
/
2003.10a
/
pp.107-107
/
2003
The activation of protooncogenes or the inactivation of their gene products may be a specific and effective functional study for human neoplasia. To examine this possibility, we have used the tetracycline regulatory system to generate transgenic mice that conditionally express the HccR-2 protooncogene in vivo. The new human cervical cancer protooncogene (HccR-2) was detected from cervical cancer cell line. To elucidate its biological functions, we generated transgenic mice that expressed the HccR-2 gene. The sustained expression of the HccR-2 transgene culminated chronic neutrophilic leukemia (CNL). CNL is a rare chronic myeloproliferative disorder that presents as a sustained, mature neutrophilic leukocytosis with few or no circulating immature granulocytes, the absence of peripheral blood monocytosis, basophilia, or eosinophilia, and infiltration of neutrophils at the liver, spleen and kidney. Mice expressing the HccR-2 and tetracycline-transactivating protein (tTa) transgene were found to have altered myeloid development that was characterized by increased percentages of mature neutrophil and band form neutrophil in the peripheral blood, liver and spleen. Activation of the transgene causes CNL. In our model, expression of HccR-2 transgene mice was similar in many respects to the human CNL. This model will be valuable not only for investigating the biological properties of the HccR-2 and other protooncogenes in vivo but also for analyzing the mechanism involved in the progression of CNL.
The apoptogenic effect of p-coumaric acid, a phenolic acid found in various edible plants, on human acute leukemia Jurkat T cells was investigated. Exposure of Jurkat T cells to p-coumaric acid (50-$150{\mu}M$) caused cytotoxicity and TdT-mediated dUTP nick-end labeling (TUNEL)-positive apoptotic DNA fragmentation along with Bak activation, ${\Delta}{\psi}m$ loss, activation of caspase-9, -3, -7, and -8, and PARP degradation in a dose-dependent manner. However,these apoptotic events were completely abrogated in Jurkat T cells overexpressing Bcl-2.Under these conditions, necrosis was not accompanied. Pretreatment of the cells with the pan-caspase inhibitor (z-VAD-fmk) could prevent p-coumaric acid-induced sub-$G_1$ peak representing apoptotic cells, whereas it failed to block ${\Delta}{\psi}m$ loss, indicating that the activation of caspase cascade was prerequisite for p-coumaric acid-induced apoptosis as a downstream event of ${\Delta}{\psi}m$ loss. FADD- and caspase-8-positive wild-type Jurkat T cell clone A3, FADD-deficient Jurkat T cell clone I2.1, and caspase-8-deficient Jurkat T cell clone I9.2 exhibited similar susceptibilities to the cytotoxicity of p-coumaric acid, excluding an involvement of Fas/FasL system in triggering the apoptosis. The apoptogenic activity of p-coumaric acid is more potent in malignant Jurkat T cells than in normal human peripheral T cells. Together, these results demonstrated that p-coumaric acid-induced apoptogenic activity in Jurkat T cellswas mediated by Bak activation, ${\Delta}{\psi}m$ loss, and subsequent activation of multiple caspases such as caspase-9, -3, -7, and-8, and PARP degradation, which could be regulated by anti-apoptotic protein Bcl-2.
Kim, Yong-Ho;Kim, Dong-Seon;Woo, Sung-Sick;Kim, Hyun-Hee;Lee, Young-Sang;Kim, Hee-Seon;Ko, Kwang-Oh;Lee, Seuk-Ki
KOREAN JOURNAL OF CROP SCIENCE
/
v.53
no.4
/
pp.407-412
/
2008
Anthocyanin pigments in soybean seed coat were D3G (Delphinidin-3-glucoside), C3G (Cyanidin-3- glucoside) and Pt3G (Petunidin-3-glucoside), which have been known potential roles in the prevention and treatment of chronic diseases. Anthocyanin contents in seed coat of blck soybean were significantly different according to soybean variety, C3G content showed the highest value in all materials and its variation was also wide. Antioxidant activity of each pigment was analyzed by DPPH and TEAC methods in which D3G and C3G showed high activity. And this study was carried out to investigate the effects of anthocyanin to human cancer cells. Cytotoxity were analyzed by MTT assay after anthocyanin pigments treated on leukemia (Jurkat T) and adenocarsinoma (MCF-7) cells. It showed decrement of cell numbers as anthocyanin concentration is increasing. ${EC}_50$ range of anthocyanin concentrations were $100{\sim}250\;ug/mL$ and $100{\sim}250\;ug/mL$ in Jurkat T and MCF-7 cell, respectively. D3G showed higher cytotoxicity than other pigments in Jurkat T cell whereas activity of C3G was high in MCF-7 cell. It is believed that supplementation of human diets with soybean anthocyanin markedly reduces human cancer mortality rates.
Journal of the Korean Society of Food Science and Nutrition
/
v.40
no.9
/
pp.1201-1207
/
2011
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been proposed as a potent tool to trigger apoptosis in cancer therapy. However, as many types of cancer cells remain resistant towards TRAIL-induced cytotoxicity, several combined therapy approaches aimed to sensitize cells to TRAIL have been developed. Genistein, a natural isoflavonoid phytoestrogen, has been shown to have anticancer activity by inducing cell cycle arrest at G2M phase as well as apoptosis in various cancer cell lines. In the present study, we showed that treatment with TRAIL in combination with subtoxic concentrations of genistein sensitized U937 human leukemia cells to TRAIL-mediated apoptosis. Combined treatment with genistein and TRAIL effectively activated caspases through Bid truncation (tBid) and down-regulation of cellular caspase-8 (FLICE)-like inhibitory proteinL ($cFLIP_L$). However, the apoptotic effects of co-treatment with genistein and TRAIL were significantly inhibited by specific caspase inhibitors, which demonstrates the important role of caspases in apoptosis induced by genistein and TRAIL. Overall, our results indicate that genistein can potentiate TRAIL-induced apoptosis through down-regulation of $cFLIP_L$ and up-regulation of pro-apoptotic tBid proteins.
$\rho$-Fluorophenylalanine (FPA), a phenylalanine analog, is able to induce apoptotic cell death of human acute leukemia Jurkat T cells. To better understand the mechanism by which FPA induces apoptotic cell death, the effect of ectopic expression of antiapoptotic proteins, Bcl-2 and Bcl-xL, on FPA-induced apoptosis was investigated by employing lurkat T cells transfected with Bcl-2 gene (JT/Bcl-2) or Bcl-xL gene (1/Bcl-xL) and Jurkat T cells transfected with vector (JT/Neo or J/Neo). When Jurkat T cells, JT/Neo or J/Neo, were exposed to FPA at concentrations ranging from 0.63 to 5.0 mM, the cell viability determined by MTT assay declined in a dose-dependent manner. In addition, apoptotic DNA fragmentation along with several apoptotic events such as caspase-8 activation, Bid cleavage, mitochondrial cytochrome c release, caspase-9 activation, caspase-3 activation, and degradation of PARP was induced. However, the FPA-induced cytotoxic effect, activation of caspase-8, and cleavage of Bid were significantly abrogated by ectopic expression of Bcl-2 or Bcl-xL. At the same time, there was marked reduction in the level of cytochrome c release from mitorhondria, caspase-9 activation, caspase-3 activation, and degradation of PARP. These results indicate that caspase-8 activation, Bid cleavage, and mitochondrial cytochrome c release with subsequent activation of the caspase cascade are negatively regulated by Bcl-2 or Bcl-xL, and are thus required for FPA-induced apoptosis in Jurkat T cells
Roolf, Catrin;Saleweski, Jan-Niklas;Stein, Arno;Richter, Anna;Maletzki, Claudia;Sekora, Anett;Escobar, Hugo Murua;Wu, Xiao-Feng;Beller, Matthias;Junghanss, Christian
Biomolecules & Therapeutics
/
v.27
no.5
/
pp.492-501
/
2019
Nitrogen-containing heterocycles such as quinoline, quinazolinones and indole are scaffolds of natural products and have broad biological effects. During the last years those structures have been intensively synthesized and modified to yield new synthetic molecules that can specifically inhibit the activity of dysregulated protein kinases in cancer cells. Herein, a series of newly synthesized isoquinolinamine (FX-1 to 8) and isoindoloquinazolinone (FX-9, FX-42, FX-43) compounds were evaluated in regards to their anti-leukemic potential on human B- and T- acute lymphoblastic leukemia (ALL) cells. Several biological effects were observed. B-ALL cells (SEM, RS4;11) were more sensitive against isoquinolinamine compounds than T-ALL cells (Jurkat, CEM). In SEM cells, metabolic activity decreased with $10{\mu}M$ up to 26.7% (FX-3), 25.2% (FX-7) and 14.5% (FX-8). The 3-(p-Tolyl) isoquinolin-1-amine FX-9 was the most effective agent against B- and T-ALL cells with IC50 values ranging from 0.54 to $1.94{\mu}M$. None of the tested compounds displayed hemolysis on erythrocytes or cytotoxicity against healthy leukocytes. Anti-proliferative effect of FX-9 was associated with changes in cell morphology and apoptosis induction. Further, influence of FX-9 on PI3K/AKT, MAPK and JAK/STAT signaling was detected but was heterogeneous. Functional inhibition testing of 58 kinases revealed no specific inhibitory activity among cancer-related kinases. In conclusion, FX-9 displays significant antileukemic activity in B- and T-ALL cells and should be further evaluated in regards to the mechanisms of action. Further compounds of the current series might serve as templates for the design of new compounds and as basic structures for modification approaches.
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