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PubMed1980

Effects of a tumor promoter and an anti-promoter on spontaneous and UV-induced 6-thioguanine-resistant mutations and sister-chromatid exchanges in V79 Chinese hamster cells.

The effects of a tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) and/or an anti-promoter antipain (protease inhibitor) on spontaneous and ultraviolet-induced sister-chromatid exchanges (SCEs) and 6-thioguanine-resistant (6TGr) recessive mutations were examined in V79 Chinese hamster cells in culture. TPA and/or antipain neither significantly altered base-line and UV-induced immediate SCE frequencies, nor decreased the level of delayed SCEs which persisted 6-7 days after irradiation. TPA and/or antipain appeared to enhance the recovery of UV-induced 6TGr colonies at the plateau expression phase despite non-mutagenicity by themselves and unaltered metabolic cooperation. Thus, the results conceivably imply that the 6TGr-recessive mutation expression, but not fixation, can be modulated at the cell level by TPA and/or antipain. Our results, together with the recent results of Loveday and Latt, may argue against the notion that TPA enhances the antipain-suppressible SCEs as an index of mitotic recombination in relevance with a tumor-promotion mechanism.

Animals↗
PubMed1977

The araC promoter: transcription, mapping and interaction with the araBAD promoter.

The start sites of the araC and araBAD gene messenger of E. coli were located by transcription in vitro from short DNA fragments, by high magnification electron microscopy and by genetic mapping. Transcription for these messengers proceeds in opposite directions from the start sites that are 150 base pairs apart. Transcription from the araBAD promoter requires araC protein plus arabinose and CAP protein plus cyclic AMP. In the experiments performed in vitro, inducing the araBAD promoter represses activity of the araC promoter.

Arabinose↗
PubMed1984

Promotion: is saccharin a promoter in the urinary bladder?

A review of various in vivo and in vitro studies indicates that saccharin has second-stage promoting activity in the rat bladder. In vitro, its effect on the human bladder is comparable to that on the rat bladder, and it produces marked hyperplasia of the urothelium. It is clear from the evidence available that the role of saccharin in carcinogenesis of the urinary bladder in vivo is complex. Given before initiation it may possibly act as a co-carcinogen and influence the response of the urothelium to initiating carcinogens. Post-initiation it can cause clonal expansion of preneoplastic cells, thus providing a large population of susceptible cells, which must still undergo some further genetic modification before they can express their full malignant potential. It is possible that saccharin, if present in sufficiently high concentration for a long enough time, may also catalyse this final malignant conversion. Nevertheless, saccharin is not a powerful co-carcinogen or promoting agent by comparison with classical skin promoters such as TPA, and it has been shown to affect tumour prevalence only if present in high concentrations over a prolonged period of time.

Animals↗
PubMed1999

Tumor promotion resistant cells are deficient in AP-1 DNA binding, JunD DNA binding and JunD expression and form different AP-1-DNA complexes than promotion sensitive cells.

The JB6 cell culture model is used to identify molecular determinants of susceptibility to the promotion of neoplastic transformation. Clonal variants susceptible to transformation ('P+' cells) form numerous anchorage-independent colonies in soft agar upon treatment with the phorbol ester tumor promoter TPA, whereas resistant variants ('P-' cells) do not. We now report that there is significantly less binding of activator protein-1 (AP-1) to its DNA binding site in P- cells than in P+ cells. Gel supershift assays were performed to detect association of all seven AP-1 family members with their DNA binding site in TPA-treated and -untreated P+ and P- cells. Significantly lower DNA binding and protein expression of JunD were detected in P- cells than in P+ cells. c-Jun was detected in P+, but not P-, AP-1-DNA complexes, and c-Fos was detected in P-, but not P+, AP-1-DNA complexes. These and other phenotype-specific differences in abundance and composition of AP-1-DNA complexes may play a role in the resistance of P- cells to tumor promoter-induced transformation.

Base Sequence↗
PubMed1987

Differential stimulation of mononuclear phagocyte IL 1 production and oxidative burst by tumor-promoting and non-tumor-promoting agents.

Adherent bone marrow, spleen and peritoneal mouse macrophages, as well as human peripheral blood monocytes were exposed in vitro to the phorbol ester derivatives 12-O-tetradecanoyl-phorbol-13-acetate (TPA), phorbol 13-monoacetate (PA), phorbol 12-myristate (PM), phorbol 12,13-diacetate (PDA), phorbol 12,13 dibutyrate (PDBu), TPA-20 aldehyde (TPA-AL), phorbol 12-retinoate 13-acetate (PRA), 4-alpha TPA (alpha-TPA) and to mezerein (MEZ) and aplysiatoxin (APL). The triggered macrophages/monocytes were tested for the production of an IL 1-like activity by the thymocyte proliferation assay and for H2O2 generation in a quantitative method which is based on the H2O2-mediated and horseradish peroxidase-dependent oxidation of phenol red. The results showed that strong first stage and second stage tumor promoters such as TPA, PDBu, PRA, MEZ and APL are also strong stimulators of IL 1 and H2O2 generation, whereas weak tumor promoters exhibited a low, if any, effect at all. The afore-described findings lend support to the idea that chronic inflammatory phagocytes might play a role in the tumor promoting process by furnishing both carcinogenic and growth factors at the site of tumor origin.

Animals↗
PubMed1998

Influence of diet restriction and tumor promoter dose on cell proliferation, oxidative DNA damage and rate of papilloma appearance in the mouse skin after initiation with DMBA and promotion with TPA.

The mouse skin tumor initiation-promotion model was used to investigate the protective effect of diet restriction in mechanistic and quantitative terms. A total of five groups of 14 male NMRI mice were initiated with 100 nmol 7,12-dimethylbenz[a]anthracene (DMBA) and promoted twice weekly with 2.5, 1.25, or 0.625 nmol 12-O-tetradecanoylphorbol-13-acetate (TPA). Food intake was ad libitum (all 3 TPA dose levels) or restricted to 70% (high and intermediate TPA dose levels). Time of appearance of the first papilloma was recorded for each mouse. Two weeks later, an osmotic minipump delivering 5-bromo-2'-deoxyuridine (BrdU) was implanted and the mouse was killed after 24 h. Cell proliferation in the epidermis was assessed by immunohistochemistry for BrdU incorporated into DNA. 8-hydroxy-2'-deoxyguanosine (8-OH-dG) in epidermal DNA was determined by HPLC/electrochemical detection. The median latency time (t50) for the appearance of skin papilloma in the high-, intermediate-, and low-dose TPA groups fed ad libitum was 9, 15.5, and 23.5 weeks, respectively. The diet-restricted groups (high and intermediate TPA dose) showed t50 values of 16 and 26 weeks. Therefore, diet restriction to 70% had approximately the same protective effect as reducing the dose of TPA by a factor of two. Both the rate of cell proliferation and the level of 8-OH-dG in the epidermis increased with the dose of TPA. Median values were increased 3- to 4-fold at the highest dose. In controls, but not in TPA-treated animals, diet restriction resulted in a decrease for both markers, by 25 and 40% for the labeling index for cell division and the level of 8-OH-dG, respectively. Both markers showed an inverse relationship with the median papilloma latency time. On an individual basis, the correlation was significant in some groups, but only for the labeling index. The data indicate that protection from the skin tumor-promoting effect of TPA by diet restriction could be based more on a reduction of the rate of cell division than on a reduction of oxidative DNA damage.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2006

Transcription regulation from a TATA and INR-less promoter: spatial segregation of promoter function.

The mode of regulation of class II genes that lack the known core promoter elements is presently unclear. Here, we studied one such example, the murine CD80 gene. An unusual mechanism was revealed wherein the pre-initiation complex (PIC) first assembled on an upstream, NF-kappaB enhancer element. Notably, this assembly occurred independent of contributions from the core promoter domain, and resulted in a PIC that was competent for transcription initiation. Positioning was subsequently achieved by exploiting the intrinsic architecture of the promoter, by virtue of which the tethered PIC was spatially juxtaposed with the transcription initiation site. Bridging interactions then ensued, through protein-protein contacts, which then enabled the elongation phase of CD80 transcription.

Animals↗
PubMed1994

Retinoic acid nuclear receptors and tumor promotion: decreased expression of retinoic acid nuclear receptors by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate.

During studies to determine the mechanism of tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA), we found that TPA downregulates mouse epidermal retinoic acid nuclear receptors (RAR), a superfamily of nuclear steroid/thyroid receptors implicated in mediating effects of retinoic acid (RA). Application of TPA to mouse skin decreased the binding of [3H]RA to RAR from mouse epidermal nuclear extracts. In this experiment, 20 nmol of TPA was applied to mouse skin and 3.5 h later binding of [3H]RA to RAR was analyzed by chromatography on a size-exclusion column. TPA treatment resulted in an approximately 67% decrease in the specific binding of [3H]RA to RAR. In a more detailed time course, application of 20 nmol of TPA to mouse skin led to 20, 36, 92 and 0% decrease in the binding of [3H]RA to mouse epidermal RAR at 2, 4, 12 and 72 h after treatment respectively. Okadaic acid, an inhibitor of protein phosphatases 1 and 2A but a mouse skin tumor promoter, also inhibited the binding of RA to RAR. RAR alpha and RAR gamma, but not RAR beta mRNA, could be detected in mouse epidermis. In addition, RA nuclear receptor RXR alpha was also expressed in the mouse epidermis. As determined by Northern blot analysis of total as well as poly(A)+ RNA, application of 10 nmol of TPA to mouse skin led to decreased expression of RAR alpha, RAR gamma and RXR alpha mRNA at 3.5 h after treatment. The effect of TPA on the attenuation of RAR expression was specific. Specific binding of RA to RAR was decreased when TPA-induced expression of the c-fos, c-jun and ornithine decarboxylase gene was increased. Downregulation of RAR(s) may be an essential component of the mechanism of mouse skin tumor promotion.

Animals↗
PubMed1986

Effects of anti-promoters and strain of mouse on tumor promoter-induced oxidants in murine epidermal cells.

The induction of oxidant production in mouse epidermal cells by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) can be suppressed by many, but not all, known inhibitors of mouse skin tumor promotion. Members of the anti-oxidant category that were tested were ranked in the following order, 7,8-benzoflavone greater than butylated hydroxyanisole greater than ascorbic acid. In the retinoid category, retinoic acid was only moderately effective, while the trimethoxymethylphenyl analog had at least twice the inhibitory activity. Among the six protease inhibitors examined, tosylphenylalanine chloromethylketone and tosyllysine chloromethylketone were effective in diminishing the response while tosylarginine methylester, antipain, leupeptin and soybean trypsin inhibitor were ineffective, suggesting that proteases are probably not involved in the oxidant response. Several agents, trifluoperazine, trisialoganglioside and diolein, that have been shown to suppress TPA activity in other cell systems were also found to suppress the oxidant response. Finally, the extent of the oxidant response was found to correlate with sensitivity to TPA tumor promotion among the three strains of mice tested: SSIn greater than SENCAR greater than C57BL/6J.

Animals↗
PubMed1982

The nucleotide sequence of the bacteriocin promoters of plasmids Clo DF13 and Co1 E1: role of lexA repressor and cAMP in the regulation of promoter activity.

Treatment of cells, harbouring the bacteriocinogenic plasmic Clo DF13 with mitomycin-C, which induces the cellular SOS response, results in a significantly increased transcription of the operon encoding the bacteriocin cloacin DF13, the immunity protein and the lysis protein H. The nucleotide sequences of the promoter regions and N-terminal parts of the bacteriocin genes of Clo DF13, Col E1 and the pMB1 derivative pBR324 have been determined. A comparison of these sequences with those of corresponding regions of the lexA, recA and uvrB genes revealed that the promoter regions of the bacteriocin genes studied contain binding sites for the lexA protein, which is the repressor of the E. coli DNA-repair system. Using both, a thermosensitive lexA host strain and a host with pACYC184 into which the lexA gene had been cloned, we were able to demonstrate, that in vivo the lexA protein is involved in the regulation of bacteriocin synthesis. From the data presented, we conclude that bacteriocin synthesis is controlled at least by the lexA repressor. It has been reported that also catabolite repression might play an essential role in the control of bacteriocin synthesis. Computer analysis of the DNA sequence data indicated that the promoter regions of both, the cloacin DF13 and colicin E1 genes contain potential binding sites for the cyclic AMP-cyclic AMP Receptor Protein complex.

Antibiotics, Antineoplastic↗
PubMed1983

Determination of the promoter strength in the mixed transcription system: promoters of lactose, tryptophan and ribosomal protein L10 operons from Escherichia coli.

In vitro transcription was performed in a single reaction mixture, which contained three species of truncated E. coli DNA template, each carrying one specific promoter, lacP (UV5), trpP or rplJp, and the transcripts of distinct sizes were analyzed by electrophoresis on the same gel. Using this "mixed transcription" system, the order of the promoter strength, i.e., the capacity to form stable open complex, was determined in the single-round transcription under the standard conditions (50 mM NaCl and 37 degrees C) to be lacP greater than trpP greater than rplJp, the latter two promoters being 30--40% and 5--10% the strength of lacP, respectively. After the multiple-round transcription, however, the level of trp transcription was the lowest due to low cyclic-reaction rate but became the highest when another trp fragment containing the natural terminator was used as the template. The order of the transcription level also varied depending on the ionic strength and the reaction temperature and, as a result, lacP was no more the strongest under high salt concentration and at high temperature.

Base Composition↗
PubMed1984

Effect of the replacement of pRoR promoter of lambda dv plasmid by lac promoter on the synthesis of DNA.

Derivatives of lambda dv whose pRoR promoter was replaced by lactose operon (lac promoter) were constructed and cloned in pBR322 plasmid. They were named pLOP-1, 2, and 3, and their structures are shown in Fig. 1. These plasmids were introduced into Escherichia coli (E. coli) lac iq and the effect of the inducer of lac promoter on the synthesis of plasmid DNA was examined. The synthesis of pLOP-2 or 3 DNA was strongly stimulated. pLOP-1, however, responded poorly to the inducer. Plasmids pLOP-2 and 3 were not segregated evenly into daughter cells after the induction and most of the progeny cells did not receive the plasmid. The synthesis of plasmid DNA after induction depended on the function of O and P genes and was inhibited by the addition of rifampicin and chloramphenicol. Most of the plasmid DNA synthesized after the induction cosedimented with the folded host chromosomal complex, suggesting an unusual structure of the DNA. When the inducer was removed, normal segregation of the plasmid resumed and the copy number of plasmid DNA decreased to the original level.

Cloning, Molecular↗
PubMed1996

Activation of S-phase-promoting CDKs in late G1 defines a "point of no return" after which Cdc6 synthesis cannot promote DNA replication in yeast.

In eukaryotic cells, DNA replication is confined to a discrete period of the cell cycle and does not usually recur until after anaphase. In the budding yeast Saccharomyces cerevisiae, assembly of pre-replication complexes (pre-RCs) at future origins as cells exit mitosis (or later during G1 is necessary for subsequent initiation of DNA replication triggered by activation in late G1 of Cdc28/Cdk1 kinases associated with B-type cyclins Clb1-Clb6. The absence of pre-RCs during G2 and M phases could explain why origins of DNA replication fire only once during the cell cycle, even though S-phase-promoting Cdks remain active from the beginning of S phase through the end of M phase. Formation of pre-RCs and their maintenance during G1 depend on the synthesis and activity of an unstable protein encoded by CDC6. We find that Cdc6 synthesis can only promote DNA replication in a restricted window of the cell cycle: between destruction of Clbs after anaphase and activation of Clb5/ and Clb6/Cdk1 in late G1. The latter corresponds to a "point of no return," after which Cdc6 synthesis can no longer promote DNA replication. Cdc6 protein can be made throughout the cell cycle and, in certain circumstances, can accumulate within the nuclei of G2 and M phase cells without inducing re-replication. Thus, control over Cdc6 degradation and/or nuclear localization is not crucial for preventing origin re-firing. Our data are consistent with the notion that cells can no longer incorporate de novo synthesized Cdc6 into pre-RCs once C1b/Cdk1 kinases have been activated. We show that Cdc6p associates with Clb/Cdk1 kinases from late G1 until late anaphase, which might be important for inhibiting pre-RC assembly during S, G2, and M phases. Inhibition of pre-RC assembly by the same kinases that trigger initiation explains how origins are prevented from re-firing until Clb kinases are destroyed after anaphase.

Anaphase↗
PubMed1997

Suppressive effects of S-methyl methanethiosulfonate on promotion stage of diethylnitrosamine-initiated and phenobarbital-promoted hepatocarcinogenesis model.

Modifying effects of S-methyl methanethiosulfonate (MMTS) on diethylnitrosamine (DEN)-initiated and phenobarbital (PB)-promoted hepatocarcinogenesis were examined in rats. Five-week-old male F344 rats were divided into 8 groups. After a week, groups 1-5 were given DEN (100 mg/kg body weight, i.p.) once a week for 3 weeks, whereas groups 6-8 received vehicle treatment. Group 2 was given 100 ppm MMTS containing diet in the initiation phase. From 4 weeks after the start of experiment, groups 3 and 5 were fed MMTS, and groups 1-3 and 7 received drinking water containing 500 ppm PB. Group 6 was given MMTS diet alone throughout the experiment (24 weeks). The incidences of hepatocellular adenoma and total liver tumors were significantly smaller in group 3 than those of group 1. The average numbers of hepatocellular adenoma, carcinoma and total tumors in group 3 were significantly smaller than in group 1. Glutathione S-transferase placental form-positive foci were also significantly decreased by MMTS treatment in the promotion phase. MMTS treatment in the initiation or promotion phase reduced ornithine decarboxylase activity in the liver of rats given DEN. The antioxidant activity against lipid peroxidation of MMTS was confirmed in tests with rabbit erythrocyte membrane ghosts or rat hepatocytes. These results suggest that MMTS is a promising chemopreventive agent for liver neoplasia when concurrently administered with PB.

Animals↗
PubMed1988

Un-health promotion: results of a survey of alcohol promotion on television.

To estimate how widely and to whom alcoholic drinks are promoted 1258 television advertisements were studied over a 10 week period that included the Christmas and New Year holidays in 1986-7. A total of 156 advertisements (12%) promoted alcohol, and this percentage increased significantly over the holiday period to 17%. These advertisements were longer than those advertising other products, and just over half (56%) occupied the first position in commercial breaks. During sports programmes and between the hours of 1800 and 1900 there was an increase in the number of advertisements for alcohol, but there was no difference before and after 2100. It was found that the extent and influence of the promotion of alcohol were great and that such advertising is seen by many children and adolescents.

Advertising↗
PubMed1996

Rhizobium leguminosarum as a plant growth-promoting rhizobacterium: direct growth promotion of canola and lettuce.

Early seedling root growth of the nonlegumes canola (Brassica campestris cv. Tobin, Brassica napus cv. Westar) and lettuce (Lactuca sativa cv. Grand Rapids) was significantly promoted by inoculation of seeds with certain strains of Rhizobium leguminosarum, including nitrogen- and nonnitrogen-fixing derivatives under gnotobiotic conditions. The growth-promotive effect appears to be direct, with possible involvement of the plant growth regulators indole-3-acetic acid and cytokinin. Auxotrophic Rhizobium mutants requiring tryptophan or adenosine (precursors for indole-3-acetic acid and demonstrate a new facet of the Rhizobium-plant relationship and that Rhizobium leguminosarum can be considered a plant growth-promoting rhizobacterium (PGPR).

Indoleacetic Acids↗
PubMed1998

Interferon-gamma and activin A promote insulin-like growth factor-binding protein-2 and -4 accumulation by human luteinizing granulosa cells, and interferon-gamma promotes their apoptosis.

Insulin-like growth factor (IGF)-binding proteins (IGFBPs) antagonize IGF and gonadotropin actions on granulosa cells. Human atretic follicles express IGFBP-2 in granulosa cells more strongly and contain higher levels of IGFBP-2 and IGFBP-4 than healthy follicles. We studied the effects of interferon-gamma (IFN gamma) and activin A, which decrease progesterone accumulation, on granulosa cell IGFBP production and apoptosis. Conditioned media from luteinizing granulosa cells cultured with IFN gamma or activin A and/or LH were subjected to ligand blotting; northern blots of total ribonucleic acid (RNA) from these cells were probed for IGFBP-2 and -4. Apoptosis was measured by in situ DNA end labeling. LH decreased medium IGFBP-2 to 21% of the control value. Although IFN gamma did not alter basal medium IGFBP-2, in the presence of LH it increased IGFBP-2 3.4-fold, with parallel changes in messenger RNA levels. Activin A also tended to increase medium IGFBP-2 in LH-treated cultures. In conditioned medium, IGFBP-4 was consistently decreased by LH, whereas both IFN gamma and activin A increased IGFBP-4 and decreased IGFBP-4 protease activity. Both LH and IFN gamma modestly stimulated IGFBP-4 messenger RNA levels. Follistatin antagonized the action of activin A, but not that of IFN gamma. IFN gamma, but not activin A, increased granulosa cell apoptosis. In conclusion, IFN gamma produced by activated lymphocytes may decrease endogenous IGF activity through stimulation of IGFBPs and may promote apoptosis of granulosa-lutein cells in vivo and, thus, luteal regression. Activin A similarly promotes IGFBP accumulation, but it does not promote apoptosis.

Activins↗
PubMed2001

Oral administration of dimethylarsinic acid, a main metabolite of inorganic arsenic, in mice promotes skin tumorigenesis initiated by dimethylbenz(a)anthracene with or without ultraviolet B as a promoter.

Concerning arsenic-induced tumorigenesis, an animal model must be developed for understanding the mechanism of human carcinogenesis by arsenics. To determine whether orally administered dimethylarsinic acid (DMA) promotes and causes the progression of skin tumorigenesis, an animal protocol by topical application of dimethylbenz(a)anthracene (DMBA) with or without UVB, a tumor promoter, in hairless mice was used. The administration of DMA by the oral route promoted not only the formation of papillomas induced by DMBA alone but also the formation of malignant tumors induced by way of the formation of atypical keratoses by treatment with DMBA and UVB. A phenomenon, the progression of keratoses-->atypical keratoses-->squamous cell carcinomas (SCCs), observed in the present study may resemble the development of tumors in arsenic-exposed humans. We also discussed the involvement of a reactive oxygen species (ROS), e.g., the dimethylarsenic peroxy radical [(CH3)2AsOO.], produced during the metabolic processing of DMA, in skin and in multi-organ tumorigenesis.

8-Hydroxy-2'-Deoxyguanosine↗