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At least 109 records · Page 6Linked to original sources
PubMed2005

[Apoptosis of human carcinoma of mouth floor KB cells and multidrug resistant KBv200 cells induced by azide methyl anthraquinone derivative].

AIM: To determine the effects of azide methyl anthraquinone derivative (AMAD) on growth inhibition and inducing apoptosis of multidrug resistant (MDR) KBv200 cells and parental drug-sensitive KB cells. METHODS: Cytotoxicity was determined by tetrazolium (MTF) assay. Reactive oxygen species (ROS) levels and mitochondrial membrane potential (deltapsi(m)) in cells were labeled with DCFH-DA and DiOC6 and tested by flow cytometry. Annexin V stain and DNA ladder were used to examine the apoptosis of KB and KBv200 cells induced by AMAD. RESULTS: AMAD was shown to inhibit the growth of KB and KBv200 cells significantly in a concentration-dependent manner, with mean IC50 of 0.36 and 0.45 micromol x L(-1), respectively. The generation of ROS increased obviously after the cells were treated with AMAD for 12 h, up to the peak in 24 h, meanwhile the levels of deltapsi(m) were time-dependently decreased. DNA fragmentation appeared on the agarose gel. Annexin V stain showed AMAD induced apoptosis of KB and KBv200 cells also in a concentration-dependent manner. CONCLUSION: AMAD showed inhibitory effect on both MDR KBv200 cells and parental drug-sensitive KB cells. The mechanism of action was associated with the increase of the cellular ROS level and the decrease of the mitochondrial membrane potential induced by AMAD, which result in cell apoptosis.

Anthraquinones↗
PubMed1984

Adenovirus-dependent release of 51Cr from KB cells at an acidic pH.

When KB cells labeled with 51Cr (1 muCi/ml) were treated with adenovirus type 2 (Ad2) at pH 6, 51Cr was released in a concentration-dependent manner with half-maximal release at 1 microgram/ml of virus. The 51Cr release was maximum at 10 micrograms/ml and represented nearly 20% of cell-associated 51Cr. 51Cr release depended on the length of incubation with Ad2 and the pH of the medium; maximum release was at pH 6 with very little release at pH 7.5. An antiserum against the penton base of Ad2 specifically neutralized the ability of Ad2 to release 51Cr. Chloroquine up to 200 microM did not block Ad2-dependent 51Cr release. DEAE-dextran stimulated Ad2-dependent 51Cr release; 4-5-fold stimulation was observed at 50 micrograms/ml of DEAE-dextran. We have compared the ability of Ad2 to release 51Cr with its ability to disrupt endocytic vesicles. Vesicle disruption was independent of pH of the medium in the range of pH 6 to 7.5 and was blocked by chloroquine, whereas, 51Cr release was much greater at pH 6 than at pH 7.5 and was not affected by chloroquine. These results suggest that Ad2 possess a lytic activity which ordinarily lyses acidic endocytic vesicles but, if the cells are maintained at acidic pH, can also directly disrupt the plasma membrane.

ADP Ribose Transferases↗
PubMed1978

Lectin binding to mosquito Aedes aegyptii and human KB cells: structural comparisons of membrane oligosaccharides.

High capacity adsorbents for lectins, including Lotus tetragonolobus L-fucose-binding protein, were readily prepared by conjugation of monosaccharides with commercially available, epoxy-activated Sepharose. Purified, radioiodinated lectins were bound to cells of the mosquito Aedes aegyptii and of human KB tumour. Relative to human KB cells, mosquito cells bound less of lectins specific for the sugars (L-fucose and D-galactose) that are terminal residues in many mammalian glycoproteins, whereas the number of binding sites of lectins specific for core-region sugars (D-mannose and 2-acetamido-2-deoxy-D-glucose) were similar. Neuraminidase, which greatly enhanced binding of peanut agglutinin or soybean agglutinin to human KB cells, had negligible effects on binding of these lectins to mosquito cells. The comparative structures of surface oligosaccharides of mosquito and KB cells are discussed in relation to the lectin-binding studies.

Aedes↗
PubMed1998

Cytotoxic effect of pingyangmycin on cultured KB cells.

The antitumour antibiotic pingyangmycin (PYM; bleomycin A5) was isolated from many components of bleomycin (BLM) produced by Streptomyces pingyangensisn. PYM has a similar chemical structure to that of BLM but the terminal amine moiety is different. Therefore, it would be of significance to demonstrate the antitumour effect and action mechanism of PYM on cultivated tumour cells. In this study, we used the cell growth curve, plating efficiency, and DNA synthesis inhibition assay to demonstrate the cytotoxicity of PYM on cultured KB cells. In the meantime, the morphological variations of drug-treated cells were also observed. In addition, we used the DNA precipitation assay, a simple and rapid assay, for detecting DNA damage caused by PYM on cultured KB cells for potential genotoxicity. Our results indicate that the effect of PYM significantly inhibits the cell growth, colonyforming ability, and DNA synthesis of KB cells in a dose-dependent manner. Furthermore, when treated with 5 micrograms/ml of PYM for 24 h on cultured KB cells, DNA strand breaks can be induced (P < 0.05). Therefore, it is considered that the action mechanism of PYM is due to its ability to inhibit the synthesis of DNA and split the DNA chains.

Antibiotics, Antineoplastic↗
PubMed2006

Differences in the fatty acid composition of KB-cells and gingival keratinocytes is culture medium additive dependent.

The influence of culture medium additives foetal bovine serum (FBS), serum effective substitutes (SES) and human autologous serum on the fatty acid profile of KB-cells and human gingival keratinocytes was examined. The KB-cells were cultivated in RPMI medium added with FBS or SES and the gingival keratinocytes in D-MEM added with FBS or human autologous serum. Two days before the cells were prepared for gas chromatography (GC), the media were changed to serum- and antibiotic-free media. Whole fatty acids of the cells were analysed using GC and the fatty acid profiles were compared. KB-cells as well as gingival keratinocytes changed their fatty acid composition, according to the medium additive used. Significant differences were observed. In the case of KB-cells cultivated with SES the fatty acid changes suggest an increase of the membrane fluidity. Corresponding and significant differences were observed with gingival keratinocytes cultivated in medium added with human autologous serum: the membrane fluidity of the gingival keratinocytes was increased. It is supposed that an increased membrane fluidity caused by a different fatty acid spectrum of the host cell may relate to mechanisms of bacterial adhesion. Consequently, in vitro studies on invasion and adhesion of bacteria or virus are dependent on the medium used. Further analyses are necessary of the functional effects caused by differences in the content of specific FAs, especially with regard to the application of cultivated cells in the field of tissue engineering.

Cell Line, Tumor↗
PubMed1991

Long-lasting accumulation of vinblastine in inostamycin-treated multidrug-resistant KB cells.

Inostamycin, a novel polyether compound, reverses multidrug resistance in KB cells. The mechanism of its action was studied by use of radioactively labeled vinblastine. Inostamycin dose-dependently increased the accumulation of [3H]vinblastine in multidrug-resistant KB-C4 cells at 0.5-2 micrograms/ml, while it did not enhance accumulation in the drug-sensitive KB-3-1 cells. At a concentration of 1 microgram/ml inostamycin inhibited active [3H]vinblastine efflux from KB-C4 cells, but not from KB-3-1 cells, and inhibited [3H]vinblastine binding to KB-C4 membranes with an IC50 of 0.94 microgram/ml (1.3 microM). Furthermore, [3H]vinblastine accumulated by treatment with 1 microgram/ml of inostamycin was resistant to efflux from KB-C4 cells, even after the removal of inostamycin.

Biological Transport↗
PubMed1981

Membrane affinity and metabolism of N4-palmitoyl-1-beta-D-arabinofuranosylcytosine into cultured KB cells.

N4-Palmitoyl-1-beta-D-arabinofuranosylcytosine (N4-palmitoyl-ara-C), a lipophilic derivative of 1-beta-D-arabinofuranosylcytosine, possessed an affinity for KB cell plasma membrane. Approximately 15 to 25% of the drug incorporated into KB cells was retained in plasma membrane when the cells were treated with the drug for 1 to 32 hr at 10 microM, the concentration required for 50% inhibition of cell growth. Less than 5.3% of the drug was found in the plasma membrane when the cells were treated with 1-beta-D-arabinofuranosylcytosine. N4-Palmitoyl-ara-C in the membrane fraction cosedimented with plasma membrane in a sucrose density gradient at 4 degrees, indicating a close association between the drug and the membrane. The affinity of N4-palmitoyl-ara-C for plasma membrane probably contributes to the efficient uptake rate and the strong cytotoxic effect of N4-palmitoyl-ara-C reported previously. The metabolites of N4-palmitoyl-ara-C in KB cells, treated with the drug for 32 hr at the concentration required for 50% inhibition of cell growth (10 microM), were analyzed by diethylaminoethyl Sepharose CL-6B column chromatography and thin-layer and paper chromatography. This analysis showed that over 98% of the drug present in the KB cell was N4-palmitoyl-ara-C. The active metabolites, 1-beta-D-arabinofuranosylcytosine, 1-beta-D-arabinofuranosylcytosine 5'-monophosphate, N4-palmitoyl-1-beta-D-arabinofuranosylcytosine 5'-monophosphate, and 1-beta-D-arabinofuranosylcytosine 5'-triphosphate, were found in amounts of 0.41, 0.37, 0.17, and 0.05%, respectively, of the total drug found in the cells. Also found were the inactive metabolites 1-beta-D-arabinofuranosyluracil and 1-beta-D-arabinofuranosylcytosine diphosphate choline in amounts of 0.61 and 0.29%, respectively.

Animals↗
PubMed2000

[Study on the relationship between the abnormal expression of c-myc and multidrug resistance in KB cell lines].

OBJECTIVE: To investigate the relationship between expression of c-myc and the regulation of mdr1, and find out the best way for gene therapy of the proliferative diseases with c-myc overexpression and reverse the multidrug resistance phenotype. METHODS: The changes of c-Myc protein and P-gp in the KB cell lines were detected by using immunohistochemistry and flow cytometry methods before and after treatment with anti-mdr1- ribozyme. RESULTS: All KB cell lines could express c-Myc protein. The expression of c-myc in multidrug resistant cell KBv displayed higher than that in sensitive cell KB. However, after reversing the multidrug resistance phenotype by anti-mdr1-ribozyme, the level of c-Myc protein expression was lower in KBv/5mR3 and KB/5mR3. The level of P-gp expression was lower in KBv/5mR3 than that in KBv but no difference in KB/5mR3 and KB. CONCLUSION: There are a close relationship between Myc protein and MDR phenotype. The c-myc involves in regulating expression of mdr1. Myc protein can be used as a new assistant implement to monitor the formation of MDR.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed1975

Nuclear deoxyribonucleic acid polymerase. Further observations on the structure and properties of the enzyme from human KB cells.

At low ionic strength KB cell DNA polymerase N1 forms large aggregates of a size comparable to those of DNA polymerase C. However, in contrast to polymerase C, the polymerase N1 aggregate: (a) retains the distinctive features of the polymerase N1 monomer, specifically its relative insensitivity to salt and to p-hydroxymercuribenzoate, and its pI of 9.3; and (b) is quantitatively converted to the polymerase N1 monomer form at appropriate ionic strength. It is important to recognize that since both polymerase N1 and polymerase C undergo salt-dependent association-dissociation reactions, attempts to distinguish these clearly indedependent polymerase species on the basis of size criteria can be very misleading. This is particularly true in relatively impure enzyme fractions that are generally isolated from eukaryotic tissue sources in low ionic strength buffers. We had earlier reported (Wang, T. S.-F., Sedwick, W. D., and Korn, D. (1974) J. Biol. Chem. 249,841-850; Sedwick, W. D., Wang, T. S.-F., and Korn, D. (1972) J. Biol. Chem. 247,5026-5033; Sedwick, W. D., Wang, T. S.-F., and Korn, D. (1974) Methods Enzymol. 29, 89-102) that DNA polymerase N1 could not utilize homoribopolymer templates. We have re-examined this question with a modified and more stringent method of product assay, and we show here that a greater than or equal 95% homogeneous preparation of polymerase N1 can copy the primer-template (A)n-(dT)-/16 at about one-half the rate that it copies activated DNA under optimum incubation conditions.

Cell Line↗
PubMed1993

Brefeldin A protects ricin-induced cytotoxicity in human cancer KB cell line, but not in its resistant counterpart with altered Golgi structures.

Brefeldin A (BFA), an isoprenoid fungal metabolite, dramatically disrupts intracellular protein transport and protein secretion. BFA protects cells from the cytotoxicity of a plant toxin, ricin or pseudomonas toxin, but not that of diphtheria toxin (Yoshida et al., 1991. Expt. Cell Res., 192: 389-395.). In this study, we examined whether BFA could differentially change the cytotoxicity of ricin between BFA-sensitive cells and BFA-resistant cells. As a BFA-resistant cell line, we used a resistant cell line, KB/BF2-2, derived from BFA-sensitive human cancer KB cells. BFA treatment caused the disappearance of typical Golgi cisternae and the concomitant appearance of dilated vesicles in the cytoplasm in KB cells. By contrast, KB/BF2-2 cells had already altered Golgi structures with poor development of cisternae and also many vesicles in the absence of BFA, and BFA treatment did not further induce the morphological changes. Although a plasma membrane-specific marker protein, alpha-adaptin, was localized similarly in KB/BF2-2 as KB, Golgi specific markers such as beta-cop and gamma-adaptin were distributed in the cytoplasmic small vesicles as well as Golgi compartments in KB/BF2-2 cells in the absence of BFA, and the mutant cells showed no apparent changes in the distribution even when exposed to BFA. Ricin inhibited protein synthesis in KB and KB/BF2-2 to similar levels while pretreatment of KB cells with BFA at 0.1 microgram/ml almost completely reversed the inhibitory effect of ricin. By contrast, the pre-exposure of KB/BF2-2 cells to 1.0 microgram/ml BFA only partially rescued the ricin-induced inhibition of protein synthesis. Exposure to BFA at 30 min before ricin addition or at 0 min with ricin rescued the protein synthesis inhibition, but no rescue occurred when BFA was added 30 min after ricin addition. BFA could not rescue the protein synthesis inhibition by another toxin, diphtheria toxin. Our results suggest that BFA-resistant mutation causes a specific change in the endocytic membrane traffic of ricin in human cells, and also that cytotoxicity of diphtheria toxin does not share a common pathway of the intracellular transport with that of ricin.

Adaptor Protein Complex gamma Subunits↗
PubMed1991

Effect of 4 beta-arylamino derivatives of 4'-O-demethylepipodophyllotoxin on human DNA topoisomerase II, tubulin polymerization, KB cells, and their resistant variants.

Six 4 beta-arylamino derivatives of 4'-O-demethylepipodophyllotoxin were examined for inhibitory activity against human DNA topoisomerase II and tubulin polymerization, their ability to generate protein-linked DNA breaks in cells, and their cytotoxicity toward the KB cell line and its VP-16- and vincristine-resistant variants. Five of these derivatives were 5- to 10-fold more potent than VP-16 as inhibitors of DNA topoisomerase II in vitro, and all of these derivatives could generate the same amount of or more protein-linked DNA breaks in cells than VP-16 at 1-20 microMs. Tubulin polymerization was inhibited by these compounds to different degrees in the order: podophyllotoxin greater than W73 greater than W87 greater than NPF greater than NPC greater than W68 greater than W38 greater than VP-16. These analogues were cytotoxic not only to KB cells but also to their VP-16-resistant and vincristine-resistant variants which showed decreased cellular uptake of VP-16 and a decrease in DNA topoisomerase II content or overexpression of MDR1 phenotype. These characteristics may cause these derivatives to have different spectrums of antitumor activity.

DNA Damage↗
PubMed1990

Correlation of protein kinase C translocation, P-glycoprotein phosphorylation and reduced drug accumulation in multidrug resistant human KB cells.

Treatment of drug-resistant human KB carcinoma cells (KB-V1) with 0.2 microM phorbol 12-myristate 13-acetate (PMA) resulted in increases of 4-fold in both membrane-associated protein kinase C activity and phosphorylation of P-glycoprotein. The response was essentially complete after 30 min and was relatively stable, since both of these parameters remained elevated above basal levels in cells exposed to PMA for 24 hours. In contrast, long-term PMA treatment of drug-sensitive KB-3 cells caused complete depletion of protein kinase C. The rate of accumulation of [3H]vinblastine in KB-V1 cells was 0.8 +/- 0.1 pmol/mg/30 min in the absence, and 1.9 +/- 0.2 pmol/mg/30 min in the presence, of 20 microM verapamil. Preincubation of cells with PMA resulted in a time-dependent decrease, up to 60% after 24 hours, in both of these values. These results suggest that protein kinase C mediated phosphorylation stimulates the drug transport activity of P-glycoprotein.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1989

[Combination effect of UFT and gamma-irradiation against nude mice transplanted KB cells].

Combination effect of UFT and gamma-irradiation was examined using KB cell transplanted in nude mice. KB cell line is known as derived from human malignant tumor of the mouth floor. Although treatment with UFT or with gamma irradiation did not suppress the tumor growth, combination of these two treatments caused a marked suppression. Especially, when UFT was administered to the mice successively from the time of transplantation and the irradiation was applied after tumor growth, both suppression of the tumor growth and necrosis of the tumor tissue were observed.

Animals↗
PubMed1985

Altered degradation of epidermal growth factor in a diphtheria toxin-resistant clone of KB cells.

We have investigated the cellular fate of epidermal growth factor (EGF) in KB cells and a variant, KB-R2A, that was isolated based on its resistance to diphtheria toxin and subsequently was shown to be resistant to infection by RNA viruses (Moehring and Moehring, 1972, Infect. Immunity. 6:487-492). Both cell lines bind 125I-EGF and internalize the cell-bound hormone at the same rate. However, when the degradation of internalized 125I-EGF was measured by the release of low molecular weight (mw) hydrolysis products into the medium, the toxin-resistant KB-R2A cells degraded the hormone at a drastically reduced rate; 50% and 3% of the cell-bound 125I-EGF was degraded and released by 80 min in the KB and KB-R2A cells, respectively. To investigate the fate of cell-associated EGF prior to release into the medium, the radioactivity in extracts of cells labeled with 125I-EGF was fractionated by native gel electrophoresis. In KB cells three peaks of radioactivity other than native 125I-EGF were resolved. Time course and subcellular fractionation studies showed that the first processed product appeared while the hormone was located in the endocytic vesicles and the appearance of the other two peaks correlated with the arrival of the hormone in the lysosomal compartment. KB-R2A cells also produced the first intermediate but they produced only very low amounts of the other two peaks. These studies show that endocytic vesicles in both cell lines contain enzymes capable of processing EGF prior to the arrival of the hormone in the lysosomes and show that the KB-R2A cells have a lesion that prevents the complete degradation of the hormone. We propose that the KB-R2A cell line has a defective mechanism for the intracellular processing of a number of ligands that are internalized by the process of receptor-mediated endocytosis and that this defect is located beyond the initial endocytic step.

Animals↗
PubMed2004

[Telomerase SiRNA inhibits KB cell growth in human oral squamous cell carcinoma].

OBJECTIVE: To test the telomerase SiRNA on telomerase mRNA and on KB cell growth of oral squamous cell carcinoma. METHODS: We synthesized 21-nucleotide SiRNA duplexes with symmetric 2-nucleotide 3' overhangs corresponding to the target sequence (2 657 approximately 2 675 nucleotide downstream of the start codon) of telomerase mRNA. Telomerase activity, cell proliferation, cell cycle and apoptosis were measured after transfection. RESULTS: Twenty one-nucleotide small interfering RNA (SiRNA) duplexes specifically suppressed expression of endogenous telomerase mRNA in human oral squamous carcinoma KB cells. This inhibitory effect lasted only for about 48 h after transfection. Telomerase activity reduction corresponded to the mRNA suppression. Cell proliferation decreased by 30% at 48 h after transfection and lasted for 120 h after treatment. This inhibitory effect resulted from the block of G(1) to S transition. Apoptosis was not involved in this process. CONCLUSIONS: SiRNA is a powerful tool for studying gene function and can be used as gene-specific therapeutics.

Apoptosis↗
PubMed2006

Porphyromonas gingivalis survives within KB cells and modulates inflammatory response.

BACKGROUND/AIMS: The purpose of the study was to investigate the intracellular survival of Porphyromonas gingivalis as a possible mechanism for maintaining periodontitis. METHODS: P. gingivalis strains, the strain ATCC 33277 and seven clinical isolates, were co-cultured with KB cells. The number of intracellular bacteria was determined up to 3 days after infection. In addition, the numbers of KB cells per well, the concentrations of the cytokines interleukin-1beta (IL-1beta), IL-6, IL-8 and tumour necrosis factor-alpha (TNF-alpha) and the arginine-specific amidolytic activity were measured. The 16S rRNA of P. gingivalis and the mRNA expression of IL-1beta, IL-6, IL-8, TNF-alpha and rgpA were also determined. RESULTS: All the P. gingivalis strains studied were able to survive within KB cells. In contrast to the reduced values of colony-forming units at day 3, equal and higher levels of 16S rRNA were seen in comparison to day 0. Arginine-specific amidolytic activity declined in all samples during infection. Expression of mRNA for rgpA was not found after infection of KB cells by P. gingivalis strains. IL-8 was detectable in all samples 2 days after infection with P. gingivalis strains. Principal components analysis underlined a correlation between the arginine-specific amidolytic activity 1 h after infection and both the released IL-8 and the mRNA expression of IL-8. Associations were found between the cultivable numbers of intracellular P. gingivalis and the mRNAs of IL-1, IL-6 and TNF-alpha at the day of infection. CONCLUSION: The results indicate survival of P. gingivalis within epithelial cells, possibly in a non-cultivable stage. Invasion into cells modulates the virulence properties of P. gingivalis as well as the inflammatory response of the cells.

Adhesins, Bacterial↗
PubMed2002

The preferential induction of apoptosis in multidrug-resistant KB cells by 5-fluorouracil.

It has been previously been shown that multidrug resistance may be associated with biochemical changes which increase the sensitivity of resistant cells to the induction of apoptosis by certain agents. We have shown here that 48 h exposure to 5-fluorouracil (5-FU) induces both a significantly greater proportion of apoptotic cells and much greater cleavage of the apoptosis-related protein poly-(ADP-ribose)-polymerase in the multidrug-resistant (MDR) carcinoma cell line, KB-A1, than in corresponding drug-sensitive control KB-3.1 cells. Exposure to 5-FU also reduced the level of the anti-apoptotic protein, protein kinase B, in the MDR cells, but not in the control cells.

Apoptosis↗
PubMed1983

Proof of recombination between viral and cellular genomes in human KB cells productively infected by adenovirus type 12: structure of the junction site in a symmetric recombinant (SYREC).

In previous work we have described a symmetric recombinant (SYREC1) between Ad12 DNA and human KB cell DNA. This recombinant DNA molecule has been generated during productive infection and is encapsidated into virions. From the DNA of a similar symmetric recombinant (termed SYREC2) between the left terminus of Ad12 DNA and human KB cellular DNA, the site of linkage between the two DNAs was cloned and sequenced. It was demonstrated that the first 2081 Ad12 nucleotides counting from the left viral terminus are conserved and linked to a sequence of GC-rich (70.4% G + C) KB cell DNA which occurs about 20 times per cellular genome. Except for a common 5'-CTGGC-3' pentanucleotide between the Ad12 DNA and KB cell DNA sequences, extensive patch homologies were not apparent at the site of junction. Similarly, comparisons of the deleted Ad12 DNA sequence and the cellular sequence replacing it did not reveal patch homologies. The 304 bp abutting the Ad12 terminus were shown to hybridize to KB cell DNA. These results provided definitive proof for the occurrence of recombinants between viral and cellular DNAs in human cells productively infected by Ad12 as previously shown by less direct experiments (Burger and Doerfler, 1974; Schick et al., 1976). Across the site of junction, an open reading frame exists which extends the truncated 54-kDal protein of the E1b region of Ad12 DNA for another 66 amino acids encoded by KB cellular DNA. This sequence is terminated by two UGA translational termination signals. The hypothetical protein has not yet been isolated.

Adenoviridae↗