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At least 73 records · Page 4Linked to original sources
PubMed1994

Inhibition of x-ray induced transformation and effect on myc and fos gene expression by the nucleotide analog, 2-aminopurine.

Ionizing radiation is a carcinogen that is known to induce malignant transformation of C3H/10T1/2 fibroblasts in vitro. Radiation is also known to induce c-myc expression and protease inhibitors that suppress radiation transformation reduce myc and fos gene expression. The antiproliferative protein kinase inhibitor 2-aminopurine has been shown to selectively inhibit serum induced c-fos and c-myc expression in human hemopoetic cells. The myc and fos oncogenes are thought to play a role in the regulation of cell proliferation and may be involved in early stages of carcinogenesis. We determined the ability of 2-aminopurine to affect x-ray-induced transformation in C3H/10T1/2 cells in vitro and its effect on myc and fos gene expression in these cells. Treatment with 2-aminopurine (5 x 10(-4) M) resulted in a 50-100% reduction in transformation yield when C3H/10T1/2 cells were irradiated with 6 Gy of x-irradiation. The 2-aminopurine had to be present during the post-confluent stage of cell growth in order to exert its inhibitory effect. Treatment of cells with 2-aminopurine significantly reduced the level of myc gene expression; the inhibitory effect of 2-aminopurine on fos gene expression in these cells was not statistically significant.

2-Aminopurine↗
PubMed2001

[The stimulating effects of bFGF on fibroblast function and its C-fos gene expression].

OBJECTIVE: To study the stimulating effects of basic fibroblast growth factor(bFGF) on fibroblast function and its ability to expression of c-fos gene. Furthermore, to explore the possible network action between bFGF and oncogene in modulating wound healing. METHODS: Cultured rat fibroblasts were divided into bFGF stimulating group and control group. Fibroblasts in bFGF stimulating group were treated with bFGF in a dosage of 40 ng/culture hole, while the control fibroblasts were treated with the same vehicle without bFGF. The morphology, cell vitality and their ability to express c-fos gene in the fibroblasts in both groups were studied with MTT and immunohistochemical methods. RESULTS: All fibroblasts in bFGF treated groups were enlarged and showed increased vitality with MTT method. C-fos gene expression in bFGF stimulating group was increased, especially in nucleus when compared with those in control group. CONCLUSION: The results show that the function and the ability to express c-fos gene in bFGF treated fibroblasts are enhanced. Combined with our previous studies, it may make a conclusion that there is a network regulation mechanism between growth factors and some oncogenes.

Animals↗
PubMed1995

Central glucoprivation evoked by administration of 2-deoxy-D-glucose induces expression of the c-fos gene in a subpopulation of neuropeptide Y neurons in the rat hypothalamus.

Central glucoprivation evoked by the intracerebroventricular administration of 2-deoxy-D-glucose (2DG) induces eating and suppresses growth hormone (GH) secretion in rats. To elucidate the hypothalamic mechanism of these phenomena, the induction of c-fos gene expression was examined by in situ hybridization using rats with centrally administered 2DG. Autoradiography on X-ray film showed that c-fos gene expression was transiently induced in discrete hypothalamic regions; namely the paraventricular nucleus, arcuate nucleus (ARC), the surrounding regions of the third ventricle dorsal to the ARC, and the periventricular nucleus (PeV). The time course of the expression was different in these nuclei. Double-label in situ hybridization for c-fos mRNA and neuropeptide Y (NPY) or somatostatin mRNAs revealed that 20% of the NPY neurons in the ARC expressed the c-fos gene, while a small population of somatostatin neurons (6.1% in the ARC and 2.6% in the PeV) expressed the c-fos gene following 2DG administration. Since NPY is an orexigenic neuropeptide and has an inhibitory effect on GH secretion, the data suggest that the activation of a subpopulation of NPY neurons in the ARC contributes, in part, to the increased food intake and suppression of GH secretion after central glucoprivation evoked by 2DG.

Animals↗
PubMed2005

c-Abl tyrosine kinase regulates c-fos gene expression via phosphorylating RNA polymerase II.

c-Abl tyrosine kinase, predominantly distributed in nucleus, has been implicated in many important cellular processes including the regulation of gene transcription. In this study, we showed that c-Abl promoted the transcription of c-fos gene, both exogenously and endogenously. The nuclear localization and tyrosine kinase activity of c-Abl were required for the activation of c-fos gene. c-Abl was associated with RNA polymerase II (RNAP II) in vivo and augmented the tyrosine phosphorylation of the largest subunit of RNAP II. In addition, c-Abl and RNAP II could be recruited to the region of c-fos promoter. The combined results suggest that c-Abl plays an important role in the transcriptional regulation of c-fos gene and the tyrosine phosphorylation of the largest subunit of RNAP II by c-Abl is involved in the regulating process.

Active Transport, Cell Nucleus↗
PubMed1991

The AP-1 site and the cAMP- and serum response elements of the c-fos gene are constitutively occupied in vivo.

The c-fos proto-oncogene is inducible by cAMP, phorbol esters, serum, and growth factors. The induction by cAMP is mediated by the conserved cAMP response element (CRE), while induction by phorbol esters, serum, and growth factors requires a distal element called the serum response element (SRE). In addition to these elements, a consensus AP-1 transcription factor binding site is located next to SRE. Upstream regions of the mouse and human c-fos genes were footprinted in vivo by the ligation-mediated polymerase chain (PCR). Our results show that all three elements are constitutively protected in mouse liver and lung and in cultured human A431 cells. No major change in the protection profile was detected in A431 cells following stimulation with epidermal growth factor or in mice at birth, when c-fos is known to be induced. These results suggest that the inducible cis elements of the c-fos gene are poised, ready to respond immediately to external signals.

Animals↗
PubMed1993

Signal transduction pathways of angiotensin II--induced c-fos gene expression in cardiac myocytes in vitro. Roles of phospholipid-derived second messengers.

Angiotensin II (Ang II) causes a rapid induction of immediate-early genes and hypertrophy in the cardiac myocyte. However, the signaling mechanism of Ang II-induced immediate-early gene expression in cardiac myocytes has not been characterized. Therefore, we examined signal transduction of Ang II in neonatal rat cardiac myocytes, using c-fos gene expression as a model system. Transient transfection of c-fos reporter gene constructs indicated that the serum response element is not only required but also sufficient for Ang II-induced activation of the c-fos promoter. Ang II is known to cause an increase in [Ca2+]i. We found that Ang II also causes a small increase in cAMP in cardiac myocytes. However, the Ca2+/cAMP response element of the c-fos gene was not sufficient to confer Ang II responsiveness to the c-fos promoter, and inhibitors of protein kinase A had no effects on Ang II-induced c-fos expression. On the other hand, chelating intracellular Ca2+ with BAPTA-AM inhibited Ang II-induced c-fos expression in a dose-dependent manner, suggesting that Ca2+ is required for Ang II-induced signaling. Measurements of phospholipid-derived second messengers revealed that Ang II increased production of inositol trisphosphate, diacylglycerol, phosphatidic acid, and arachidonic acids, resulting in a sustained increase in protein kinase C activity. This and other evidence suggest that Ang II activates phospholipase C, phospholipase D, and possibly phospholipase A2. All of these second-messenger systems are activated through the AT1 receptor. Pharmacological inhibition of phospholipase C or downregulation of protein kinase C significantly suppressed Ang II-induced c-fos expression. In conclusion, Ang II activates multiple phospholipid-derived second-messenger systems via the AT1 receptor in cardiac myocytes. Among these second-messenger systems, phospholipase C and protein kinase C seem essential for Ang II-induced c-fos gene expression, whereas Ca2+ may play a permissive role. Finally, the "Ang II response element" of the c-fos gene maps to the protein kinase C-dependent portion of the serum response element.

Adenylyl Cyclases↗
PubMed1989

A multiple cytokine- and second messenger-responsive element in the enhancer of the human interleukin-6 gene: similarities with c-fos gene regulation.

Interleukin-6 (IL-6) is a major systemic alarm signal that indicates the occurrence of tissue damage. The IL-6 gene is induced in various cell types by serum, inflammation-associated cytokines, viruses, and second-messenger agonists. There is an overall functional similarity between IL-6 and c-fos promoters, since transfection of excess amounts of either promoter DNA into intact HeLa cells modulates the function of the heterologous promoter construct. Furthermore, the transcription regulatory factor Fos transrepresses both the IL-6 and c-fos promoters. The 115-base pair (bp) region from -225 to -111 in the IL-6 5'-flanking region, which shares nucleotide sequence similarity with the c-fos serum response (SRE) and adjacent AP-1-like (the CGTCA motif) elements, confers responsiveness to several reagents, including serum, forskolin, and phorbol ester, upon the heterologous herpesvirus thymidine kinase (TK) promoter. In gel shift assays using nuclear extracts from HeLa cells, the 115-bp IL-6 enhancer formed several complexes that (i) were increased when extracts from induced HeLa cells were used and (ii) were inhibited most efficiently by the fos E DNA fragment (-700 to -100) and by c-fos oligonucleotides containing an intact AP-1-like site (the CGTCA motif). The 23-bp oligonucleotide designated AR1 from within the IL-6 enhancer region (-173 to -151) contains a CGTCA motif and bound nuclear proteins that also associated with c-fos oligonucleotides containing either an intact SRE or AP-1-like site. A single copy of AR1 inserted upstream of the herpesvirus TK promoter rendered this heterologous promoter inducible by IL-1 alpha, tumor necrosis factor, and serum as well as by activators of the protein kinase A (forskolin) and protein kinase C (phorbol ester) signal transduction pathways. Mutations in the AP-1-like site within AR1 (CGTCA----GTTCA) decreased inducibility of the chimeric IL-6/TK/chloramphenicol acetyltransferase gene by phorbol ester and by forskolin but not by serum, IL-1 alpha, or tumor necrosis factor. These data not only show that the AR1 segment from within the IL-6 enhancer binds nuclear proteins that also bind to c-fos regulatory elements but also demonstrate that a single copy of this 23-bp element is functionally sufficient to confer responsiveness to a variety of inducers and thus define a multiple-response element.

Base Sequence↗
PubMed2000

YM905, a novel M3 antagonist, inhibits Ca2+ signaling and c-fos gene expression mediated via muscarinic receptors in human T cells.

Our earlier observations suggest that M3 muscarinic acetylcholine (ACh) receptors (mAChRs) are involved in Ca2+ signaling and regulation of c-fos gene expression in T lymphocytes. Here, we describe the effects of YM905, a novel M3 antagonist, on evoked Ca2+ signaling and c-fos gene expression in CEM human leukemic T cells. YM905 significantly inhibited increases in intracellular free Ca2+ evoked by 10 microM oxotremorine-M, an M1/M3 agonist (IC50=100 nM), and also inhibited 10 microM oxotremorine-M-induced upregulation of c-fos gene expression at 1 microM. These findings demonstrate that YM905 antagonizes the intracellular responses in T cells induced via mAChRs, possibly M3 receptors.

Calcium Signaling↗
PubMed1991

The role of jun and fos gene family members in 12-O-tetradecanoylphorbol-13-acetate induced hemopoietic differentiation.

Terminal differentiation of the leukemic cell lines U-937 and HL-60 by 12-O-tetradecanoylphorbol-13-acetate is accompanied by marked changes in gene expression. In this study, we demonstrate that the expression of jun and fos gene family members is induced with variable kinetics during 12-O-tetradecanoylphorbol-13-acetate induced differentiation, with c-jun expression best paralleling differentiation. The generation of AP-1 complexes, as measured by DNA binding activity, closely parallels morphological differentiation. Furthermore, the ability of these complexes to regulate gene expression is demonstrated by increased transcription from an AP-1 driven reporter construct and marked increases in the expression of endogenous AP-1 regulated genes. Differentiation assays using water soluble phorbol esters reveal that differentiation becomes irreversible soon after AP-1 appears. This tight correlation between c-jun expression, the generation of AP-1 activity, and differentiation suggests a critical role for this gene and transcriptional complex during this process.

Cell Differentiation↗
PubMed1998

Suppression of c-Fos gene transcription with malignant transformation of human bronchial epithelial cells.

The Activator Protein-1 (AP-1) complex is a dimeric transcription factor composed of fos and jun proteins that regulates cellular growth and differentiation. We previously demonstrated a reduction in basal AP-1 transcriptional activity associated with the malignant transformation of human bronchial epithelial (HBE) cells that was, in part, a consequence of decreased c-fos expression. In this study, we investigated the mechanisms underlying the reduction in c-fos expression associated with the malignant transformation of HBE cells. c-Fos gene transcription was lower in tumorigenic HBE cells than in normal HBE cells, and the reduction in transcription involved c-fos gene promoter elements from -327 to +40. DNaseI footprinting and band shift analyses of motifs within this c-fos promoter region, including a cyclic AMP response element (CRE), serum response element (SRE), sis-inducible element (SIE), and a YY1 site, revealed that binding to these motifs was greater in tumorigenic HBE cells than in normal HBE cells. Site-directed mutagenesis of the CRE partially relieved the repression of c-fos promoter activity in tumorigenic HBE cells. Further, the activity of the Jun N-terminal Kinase (JNK)-dependent pathway, which was a positive regulator of the c-fos promoter, was greater in normal HBE cells than in tumorigenic HBE cells. These findings demonstrate a transcriptionally-mediated suppression of c-fos gene expression associated with the malignant transformation of HBE cells. The decreased activity of the c-fos promoter in tumorigenic 1170I cells appeared to involve suppression through a CRE site and reduced activation by JNK-dependent pathways.

Bronchi↗
PubMedDate not supplied

Expression of the c-fos gene in the mouse brain during the acquisition of defensive behavior habits.

Experimental data reported here provide evidence that marked defensive motivation in conditions of an unavoidable electrocutaneous stimulus is accompanied in mice by increases in the expression to the c-fos gene in the hippocampus and cerebral cortex. As reinforcement and learning progress and the animals become able to achieve a useful result--avoiding the electrocutaneous shock--expression of the c-fos gene in these brain structures decreases. The level of expression of the c-fos gene was found to be different in animals in which defensive behavior had different efficacies. Expression was higher in mice making large numbers of errors than in mice with few errors during acquisition of the defensive habit.

Animals↗
PubMed2001

[The effect of alcohol on c-fos gene expression in rat embryo neuroglial].

OBJECTIVE: This paper is aimed to explore the mechanisms of brain development abnormality induced by alcohol. METHODS: Astrocytes and oligodendrocytes of 19-day rat embryo were exploited and cultured in vitro, and alcohol and its metabolite product (acetaldehyde) were added to DMEMF(12) medium. After different exposure times, c-fos expression of astrocytes and oligodendrocytes was measured by the immunocytochemistry technique. RESULTS: Changes in c-fos gene expression induced by alcohol and acetaldehyde was time and dose dependent. After 1 hr exposure, alcohol and acetaldehyde affected c-fos gene expression in two kinds of neuralglia. C-fos positive expression reached peak value after 2 hr, but recovered after 72 hr and showed special time phase expression. CONCLUSIONS: Alcohol and acetaldehyde cause abnormal increase of c-fos gene expression in astrocytes and oligodendrocytes. This abnormal expression may play an important role in abnormal brain development induced by alcohol.

Acetaldehyde↗
PubMed1987

Chemoattractant-induced activation of c-fos gene expression in human monocytes.

Human monocytes use the products of phosphoinositide hydrolysis (1,2-diacylglycerol and inositol 1,4,5-triphosphate) as second messengers to trigger rapid cellular activation during the occupancy of chemoattractant receptors. The effect of chemoattractants on modulation of gene expression in monocytes was examined in this study. The chemoattractants FMLP and platelet-activating factor induced the progressive increase of c-fos RNA to 6-15-fold over those of control within 30 min after treatment. Similar kinetics of c-fos gene activation was also observed when cells were treated with PMA or sn-1,2-dioctanoylglycerol, but not with the calcium mobilizer ionomycin, suggesting a role for protein kinase C in gene regulation by chemoattractant receptors. Activation of c-fos gene expression by FMLP is mediated through a pertussis toxin-sensitive G protein, since pertussis toxin treatment of the cells blocked the induction of the c-fos gene by FMLP but not PMA. The level of c-myc RNA was slightly decreased after 1 h of treatment with chemoattractants, but not with PMA or diacylglycerol. This implies that chemoattractant receptor occupancy generates signals beyond protein kinase C activation that are capable of selectively downregulating monocyte gene expression. The effect of FMLP and PMA on the accumulation of c-fos RNA appears to result from altering both the rate of transcription and message stability. These observations indicate that signals generated through chemoattractant receptor occupancy may regulate monocyte function at the genetic level.

Cycloheximide↗
PubMed1994

Prolactin induces rapid p95/p70 tyrosine phosphorylation, and protein binding to GAS-like sites in the anx Icp35 and c-fos genes.

Several growth factors and cytokines have been proposed to act through signaling pathways related by their dependence on tyrosine phosphorylation of latent transcription factors, and their use of similar transcription factor binding sites. Related mechanisms have previously not been reported for prolactin, growth hormone, or any other glandular hormone. We have identified sequences in the annexin Icp35 gene that are related to regulatory sequences in mammary gland milk protein genes, and then used DNA binding assays to show that PRL induces transient expression of factors specific for these sequences. The sequences in question are partially related to the core homology of the interferon (IFN)gamma-activated sequence (GAS). Considering that the prolactin-regulated factors might be related to the p91 component of IFN gamma-activated factor, we used immunoassays to show that prolactin induced tyrosine phosphorylation of a protein that comigrated with immunoreactive relatives of p91, and that antibody to p91 specifically interfered with the prolactin-induced binding activity on the annexin Icp35 gene.

Animals↗