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Relevant bibliographies by topics / Modulation of oncogene expression

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Academic literature on the topic 'Modulation of oncogene expression'

Author: Grafiati

Published: 29 March 2025

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Journal articles on the topic "Modulation of oncogene expression"

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Seldin, M. F., J. D. Mountz, J. F. Mushinski, H. R. Smith, and A. D. Steinberg. "IL-2 Modulation of Murine T-Cell Oncogene Expression." Experimental Biology and Medicine 184, no. 2 (February 1, 1987): 186–90. http://dx.doi.org/10.3181/00379727-184-42465.

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Harel-Bellan, Annick, and William L. Farrar. "Modulation of proto-oncogene expression by colony stimulating factors." Biochemical and Biophysical Research Communications 148, no. 3 (November 1987): 1001–8. http://dx.doi.org/10.1016/s0006-291x(87)80231-0.

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Spirin, P. V., N. A. Nikitenko, T. D. Lebedev, P. M. Rubtsov, C. Stocking, and V. S. Prasolov. "Modulation of activated oncogene c-kit expression with RNA-interference." Molecular Biology 45, no. 6 (December 2011): 950–58. http://dx.doi.org/10.1134/s0026893311060136.

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Sarno, Federica, Désirée Goubert, Emilie Logie, Martijn G. S. Rutten, Mihaly Koncz, Christophe Deben, Anita E. Niemarkt, et al. "Functional Validation of the Putative Oncogenic Activity of PLAU." Biomedicines 11, no. 1 (December 30, 2022): 102. http://dx.doi.org/10.3390/biomedicines11010102.

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Plasminogen activator, urokinase (PLAU) is involved in cell migration, proliferation and tissue remodeling. PLAU upregulation is associated with an increase in aggressiveness, metastasis, and invasion of several cancer types, including breast cancer. In patients, this translates into decreased sensitivity to hormonal treatment, and poor prognosis. These clinical findings have led to the examination of PLAU as a biomarker for predicting breast cancer prognosis and therapy responses. In this study, we investigated the functional ability of PLAU to act as an oncogene in breast cancers by modulating its expression using CRISPR-deactivated Cas9 (CRISPR-dCas9) tools. Different effector domains (e.g., transcription modulators (VP64, KRAB)) alone or in combination with epigenetic writers (DNMT3A/3L, MSssI) were fused to dCas9 and targeted to the PLAU promoter. In MDA-MB-231 cells characterized by high PLAU expression downregulation of PLAU expression by CRISPR-dCas9-DNMT3A/3L-KRAB, resulted in decreased cell proliferation. Conversely, CRISPR-dCas9-VP64 induced PLAU upregulation in low PLAU expressing MCF-7 cells and significantly increased aggressiveness and invasion. In conclusion, modulation of PLAU expression affected metastatic related properties of breast cancer cells, thus further validating its oncogenic activity in breast cancer cells.

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Kakhlon, O., Y. Gruenbaum, and Z. I. Cabantchik. "Repression of ferritin expression modulates cell responsiveness to H-ras-induced growth." Biochemical Society Transactions 30, no. 4 (August 1, 2002): 777–80. http://dx.doi.org/10.1042/bst0300777.

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We assessed the role of the cell labile iron pool in mediating oncogene-induced cell proliferation via repression of ferritin expression. When HEK-293 cells, engineered to inducibly express either active (+) or dominant-negative (-) forms of the H-ras oncogene, were treated with antisense nucleotides to ferritin subunits they displayed (a) decreased ferritin levels, (b) increased labile iron pool and either (c) faster growth in cells induced to express H-Ras (+) or (d) recovery from growth retardation in dominant-negative H-Ras-induced cells. Our studies support the view that the role of down-modulation of ferritin expression by some oncogene-evoked proliferation proceeds via expansion of the cellular labile iron pool.

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Lehtola, L., M. Nistér, E. Hölttä, B. Westermark, and K. Alitalo. "Down-regulation of cellular platelet-derived growth factor receptors induced by an activated neu receptor tyrosine kinase." Cell Regulation 2, no. 8 (August 1991): 651–61. http://dx.doi.org/10.1091/mbc.2.8.651.

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The functional integration of growth factor signaling occurs at several levels in target cells. One of the most proximal mechanisms is receptor transmodulation, by which one activated receptor can regulate the expression of other receptors in the same cells. Well-established transregulatory loops involve platelet-derived growth factor (PDGF) down-regulation of epidermal growth factor (EGF) receptors and beta-type transforming growth factors modulation of PDGF receptors. We have studied the relationship between neu tyrosine kinase activation and the expression of the PDGF receptors in transfected NIH/3T3 cells. Expression of the neu oncogene, but not of the neu proto-oncogene, was associated with a decrease of PDGF alpha- and beta-receptors on the cell surface, as measured by [125-I]PDGF-AA and -BB binding. These results were corroborated by metabolic labeling and immunoprecipitation of the PDGF beta-receptors. PDGF alpha- and beta-receptor mRNAs were strongly decreased in the neu oncogene-transformed cells in comparison with control cells expressing the neu proto-oncogene. Down-regulation of the PDGF receptors and their mRNAs was also observed after EGF treatment of cells expressing a chimeric EGF receptor/neu receptor, where the neu tyrosine kinase is activated by EGF binding. These results show that the neu tyrosine kinase can down-modulate PDGF receptor expression, and the effect is mediated via decreased PDGF receptor mRNA levels.

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Bell, S. M., D. C. Connolly, N. J. Maihle, and J. L. Degen. "Differential modulation of plasminogen activator gene expression by oncogene-encoded protein tyrosine kinases." Molecular and Cellular Biology 13, no. 9 (September 1993): 5888–97. http://dx.doi.org/10.1128/mcb.13.9.5888-5897.1993.

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Urokinase-type plasminogen activator (uPA) gene transcription is increased > or = 50-fold in chicken embryo fibroblasts (CEF) following transformation by the protein tyrosine kinase pp60v-src. Protein phosphorylation appears to play a critical role in uPA gene expression in these cells; protein kinase C-activating phorbol esters cooperate with pp60v-src to synergistically increase uPA mRNA, whereas cyclic AMP (cAMP)-dependent protein kinase-activating agents (e.g., 8-bromo cAMP) repress uPA mRNA levels. To explore the relationship between transforming oncogenes and uPA gene expression, uPA mRNA levels were measured in CEF infected with selected avian retroviruses. We report that v-ras and the transforming protein tyrosine kinases v-src, v-yes, and v-ros all increase cellular uPA mRNAs. However, transformation with the protein tyrosine kinase encoded by v-erbB, or the nuclear proteins encoded by v-jun, v-ski, or v-myc, did not increase uPA mRNA detectably. Ras and all of the protein tyrosine kinases analyzed, including the v-erbB product, but none of the nuclear oncoproteins sensitized cells to phorbol ester induction of uPA gene expression. Thus, increased uPA gene expression is not simply a secondary consequence of cell transformation but, rather, is regulated or comodulated by only a subset of oncogene products. Analysis of cells expressing site-directed mutants of pp60v-src showed that the induction of the uPA gene is dependent on protein tyrosine kinase catalytic activity, myristylation, and plasma membrane localization. However, these properties together are not sufficient; an additional feature in the src homology 2 domain is also required. The major sites of serine phosphorylation, serines 12 and 17, and the autophosphorylation site, tyrosine 416, are not essential for uPA gene induction. However, the reduction of uPA mRNA in pp60v-src-transformed cells by 8-bromo cAMP is dependent on tyrosine 416.

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Bell, S. M., D. C. Connolly, N. J. Maihle, and J. L. Degen. "Differential modulation of plasminogen activator gene expression by oncogene-encoded protein tyrosine kinases." Molecular and Cellular Biology 13, no. 9 (September 1993): 5888–97. http://dx.doi.org/10.1128/mcb.13.9.5888.

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Urokinase-type plasminogen activator (uPA) gene transcription is increased > or = 50-fold in chicken embryo fibroblasts (CEF) following transformation by the protein tyrosine kinase pp60v-src. Protein phosphorylation appears to play a critical role in uPA gene expression in these cells; protein kinase C-activating phorbol esters cooperate with pp60v-src to synergistically increase uPA mRNA, whereas cyclic AMP (cAMP)-dependent protein kinase-activating agents (e.g., 8-bromo cAMP) repress uPA mRNA levels. To explore the relationship between transforming oncogenes and uPA gene expression, uPA mRNA levels were measured in CEF infected with selected avian retroviruses. We report that v-ras and the transforming protein tyrosine kinases v-src, v-yes, and v-ros all increase cellular uPA mRNAs. However, transformation with the protein tyrosine kinase encoded by v-erbB, or the nuclear proteins encoded by v-jun, v-ski, or v-myc, did not increase uPA mRNA detectably. Ras and all of the protein tyrosine kinases analyzed, including the v-erbB product, but none of the nuclear oncoproteins sensitized cells to phorbol ester induction of uPA gene expression. Thus, increased uPA gene expression is not simply a secondary consequence of cell transformation but, rather, is regulated or comodulated by only a subset of oncogene products. Analysis of cells expressing site-directed mutants of pp60v-src showed that the induction of the uPA gene is dependent on protein tyrosine kinase catalytic activity, myristylation, and plasma membrane localization. However, these properties together are not sufficient; an additional feature in the src homology 2 domain is also required. The major sites of serine phosphorylation, serines 12 and 17, and the autophosphorylation site, tyrosine 416, are not essential for uPA gene induction. However, the reduction of uPA mRNA in pp60v-src-transformed cells by 8-bromo cAMP is dependent on tyrosine 416.

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Codony, Carles, Sònia Guil, Concha Caudevilla, Dolors Serra, Guillermina Asins, Adolf Graessmann, Fausto G. Hegardt, and Montse Bach-Elias. "Modulation in vitro of H-ras oncogene expression by trans-splicing." Oncogene 20, no. 28 (June 2001): 3683–94. http://dx.doi.org/10.1038/sj.onc.1204473.

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Pierotti, Marco A., Maria G. Borrello, Italia Bongarzone, Maria R. Cattadori Rosangela Donghi, Piera Mondellini, Catia Traversari, and Giuseppe Della Porta. "Modulation of the human Ha--1 oncogene expression by DNA methylation." European Journal of Cancer and Clinical Oncology 23, no. 11 (November 1987): 1788–89. http://dx.doi.org/10.1016/0277-5379(87)90683-3.

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Dissertations / Theses on the topic "Modulation of oncogene expression"

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Appleby, Mark William. "Oncogene expression and the modulation of keratinocyte self renewal." Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306476.

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Cristofari, Camilla. "Non Canonical structures within MYC and BCL2 oncogenes: novel targets for gene expression modulation." Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3422715.

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Cancer diseases are increasing worldwide and more than 20 million new cancer cases per year are expected by 2025. At these days the treatment of neoplastic forms took advantage of classic approaches, based on chemotherapeutics and radiotherapeutics agents. However they are characterized by numerous limitations as remarkable side effects, toxicity and selection of resistant phenotypes to such therapies. This prompted the development of so-called targeted therapies, where selective chemical entities (small molecules, monoclonal antibodies, miRNAs, siRNAs etc.) hit a single molecular target of the tumor phenotype. Despite, these therapies have proven to be efficient alternatives they also present several limitations that make them quite ineffective. In order to overcome these remarkable drawbacks, he modulation of the gene expression, that exploits the ability of nucleic acids to assume different conformations, defined as non-canonical, became extremely interesting. Among these non-canonical conformations, extremely fascinating are the tetrahelical conformations known as G-quadruplex (G4) and i-Motif (iM), that seem to be involved in the blockage of the cancer development. G4 structures occur at DNA and RNA sequences presenting a high abundance of consecutive guanines that interact each other through Hoogstein hydrogen bonds to generate a planar structure called G-tetrads. Stacking interaction between two or more G tetrads create the overall structure. Bioinformatics studies revealed that prevalently these regions are contained along the telomeres and within the untranslated region (UTR) or within the promoter sites of several oncogenes (approximately 40%) directly implicated in the development of tumor phenotypes. The UTR domains, as the promoter regions, are double-stranded DNA sequences. Therefore the complementary strand results enriched in cytosine, that under specific environmental conditions can folds into a tetrahelical conformation, known as i-Motif. Unlike the G4s, the building block of the entire structure is a dimer of cytosine mainly stabilized by the presence of three Hoogstein hydrogen bonds. The in vivo formation of G4 and iM leads to a steric hindrance at the DNA level; this suggests an inhibition/activation effect on the elongation process of the telomere or on the gene expression process Under the supervision of Dr. Laurence J. Hurley, the structural characterization of the cytosine rich sequence contained within the NHE(III)1 region of MYC promoter was completed. In particular, was assessing the effect of the loop composition on the stability and folding process of the already characterized iM. Since it was proved that this conformation in vivo is involved in the transcriptional activation, the possibility to target it by using a selected compound (IMC-30) was considered. Furthermore, we took into consideration the possibility to use this compound (IMC-30) as an anticancer drug by testing its ability to induce the apoptosis process in a cancer cell line in which the selected gene was overexpressed. Besides the several evidence reported for the tetrahelical conformations assumed by the GC-rich promoter regions, more recently the efforts moved forward to the G-rich tract contained in the untranslated (UTR) domains, both the 5â- and the 3â-UTR, of the primary transcript. Since, they can act as modulators of the translation process. Based on this evidence, in this project, the guanine rich sequences contained in the 5'-UTR region, both at the DNA and RNA levels, of the BCL2 gene were considered. In particular, the structural characterization study was initially carried out on the minimal sequences (dBcl2_G and rBcl2_G), then the effect exerts by the presence of additional nucleotides on the folding process towards the G-quadruplex was taken into consideration (dBcl2_G + 3 WC, rBcl2_G + 3 WC and rBcl2_48). Additionally, the cytosine rich tract contained on the DNA complementary strand was considered and characterized. Our data have shown that the dBcl2_G and rBcl2_G are able to assume multiple G4 conformations. While, the presence of additional nucleotides strongly modulates their ability to assume the non-canonical conformation. Indeed, we proved that the presence of 3 WC pairing partially prevents the formation of G4 both in the DNA and in the RNA, while the addition of a greater number of bases (rBcl2_48) leads to the formation of a different conformation that competes with the G4 structure. Regarding the cytosine rich string, its conformational equilibria have been taken into consideration both in a mildly acidic environment and in an environment that mimics the physiological condition. Finally, we implemented our work, by screening a library of compounds on each tested sequences in order to find a ligand that selectively recognizes and stabilizes one conformation. From the acquired data it emerged the feasibility to stabilize/induce the iM using the Bisanthrene compound and its derivative Bis 1-8. For the guanine rich sequences, Sanguinarine and Chelerythrine provide the best results on each tested tracts, therefore they cannot be considered selective compounds. Similarly, also the Bisanthrene derivatives recognize and interact with each tested guanine tracts, although with different selectivity.
Oggigiorno una delle “piaghe” che affligge maggiormente la popolazione mondiale è il cancro. Il trattamento di queste forme neoplastiche sfrutta agenti chemioterapici e radioterapici, caratterizzati da numerose limitazioni legate ai notevoli effetti collaterali, alla tossicità e alla selezione di fenotipi resistenti a tali terapie. Ciò ha portato allo sviluppo delle targeted therapy, che sfruttano entità chimiche (small molecules, anticorpi monoclonali, miRNA, siRNA ecc.) selettive per un bersaglio molecolare caratteristico del fenotipo tumorale. Nonostante più mirati anche questi approcci presentano degli effetti collaterali Pertanto la modulazione dell’espressione genica che sfrutta la capacità degli acidi nucleici di assumere differenti conformazioni, definite non canoniche, ha destato sempre più interesse. Tra le possibili strutture non canoniche di notevole interesse sono le conformazioni tetraelicoidali note come G-quadruplex (G4) e i-Motif (iM). La struttura G4 è propria di sequenze di DNA e RNA contenenti un’elevata abbondanza di guanine consecutive che, mediante legami a idrogeno di tipo Hoogstein, generano delle strutture planari chiamate tetradi. Dall’’impilamento di due o più tetradi si genera la struttura a tetraelica. Poiché il DNA è una doppia elica, il filamento complementare a queste regioni G ricche presenta un’elevata abbondanza di citosine. Anche questi domini in particolari condizioni ambientali, possono generare una conformazione tetraelicoidale, nota come i-Motif. A differenza del G4, il building block dell’intera struttura è un dimero di citosine stabilizzato dalla presenza di tre legami a idrogeno. In vivo l’esistenza di queste conformazioni, genera una sorta d’ingombro sterico a livello del DNA e ciò presuppone un effetto d’inibizione/attivazione del processo di elongazione del telomero o del processo trascrizionale. Sotto la supervisione del Dott. Laurence J. Hurley, è stata implementata la caratterizzazione strutturale della stringa di citosine contenute nel promotore del gene MYC. In seguito un selezionato ligando è stato testato con l’idea di poter modulare il processo di folding/unfolding alla base dell’attivazione trascrizionale. Infine, l’effetto mediato da questo composto sul processo apoptotico è stato preso in considerazione lavorando su una selezionata linea cellulare. Di notevole interesse sono le regioni GC-ricche contenute nella porzione non tradotta del trascritto primario (mRNA). Sulla base di ciò, in questo progetto, sono state prese in considerazioni, le stringhe di guanina e citosina contenute nella regione del 5’-UTR, sia a livello del DNA sia del RNA, del gene BCL2. Inizialmente è stato condotto uno studio di caratterizzazione sulle sequenze minimali dBcl2_G, dBcl2_C e rBcl2_G. In seguito è stato preso in considerazione l’effetto della presenza di nucleotidi adiacenti sul processo di folding verso il G-quadruplex (dBcl2_G + 3WC, rBcl2_G + 3WC e rBcl2_48). I dati ottenuti dimostrano che le sequenze dBcl2_G e rBcl2_G sono in grado di assumere molteplici conformazioni G4. La presenza di nucleotidi addizionali modula la loro capacità di assumere queste conformazioni. In particolare, la presenza di tre appaiamenti WC impedisce parzialmente la formazione del G4 sia nel DNA, che nel RNA mentre, l’aggiunta di un maggior numero di basi (rBcl2_48) sposta l’equilibrio conformazionale verso una conformazione in forte competizione con il G4. Per la sequenza ricca di citosine, l’equilibrio conformazionale è stato valutato sia in ambiente blandamente acido, che in un ambiente che mima la condizione fisiologica. Infine, poiché negli ultimi anni è stata dimostrata la capacità di alcuni ligandi sintetici/naturali, di spostare gli equilibri conformazionali del DNA, dalla classica forma a doppio filamento, verso queste conformazioni tetraelicoidali, una selezionata libreria di composti è stata, scrinata allo scopo di individuare un ligando in grado di riconoscere e stabilizzare selettivamente una conformazione al pari di un'altra.

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Froux, Aurane. "G-quadruplex binding by transition metal complexes : the whole pathway from design to synthesis, to in cellulo anticancer investigations." Electronic Thesis or Diss., Université de Lorraine, 2024. https://docnum.univ-lorraine.fr/ulprive/DDOC_T_2024_0206_FROUX.pdf.

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Les cancers du sein triple négatifs et du pancréas sont associés à de faible taux de survie, dû à leur forte résistance aux traitements conventionnels, constituant un réel problème de santé publique et rendant le développement de nouvelles thérapies ciblées crucial. Au niveau des séquences télomériques et des promoteurs d'oncogènes comme cMYC, cKIT et BCL2, les séquences riches en guanines peuvent former des structures secondaires non conventionnelles, appelées G-quadruplexes. Ces structures jouent un rôle important dans la régulation de l'expression génique, constituant ainsi de prometteuses cibles thérapeutiques pour la lutte contre le cancer.Ici, nous avons choisi une approche pluridisciplinaire, alliant synthèse chimique, chimie théorique, et biologie cellulaire et moléculaire, afin d'identifier de nouveaux composés stabilisant ces structures, dans le but de contrôler la prolifération des cellules cancéreuses. Notre laboratoire a précédemment montré l'intérêt des complexes métalliques symétriques et planaires dans la stabilisation spécifique des G-quadruplexes. Ainsi, nous avons synthétisé 12 nouveaux complexes à base des métaux de transition Zn2+, Ni2+, Cu2+, Pd2+ et Pt2+. Leur capacité à sélectivement stabiliser les G-quadruplexes, en comparaison avec l'ADN double brin, a été démontré et des simulations de dynamique moléculaire révèlent un mode d'interaction peu conventionnel, impliquant la boucle du G-quadruplex.Nos composés induisent la formation de G-quadruplexes au sein des lignées cellulaires cancéreuses, entrainant une régulation à la baisse de nombreux oncogènes comme kRAS, RET et cMYC. Cette répression entraine une réduction de la prolifération et la viabilité des cellules cancéreuses, mais n'affecte que peu les cellules saines.Alors que certains composés induisent la mort des cellules cancéreuses par apoptose sans affecter les cellules saines, et inhibent drastiquement l'expression des oncogènes hRAS et cMYC, d'autres complexes causent des dommages à l'ADN dans les cellules néoplasiques pancréatiques T3M4. Aussi, les composés de Zn2+ favorisent l'expression de VEGF-A, en stimulant sa transcription. L'étude de l'impact d'une stabilisation des G-quadruplexes sur la polarisation des macrophages a montré que les composés de nickel promeuvent la polarisation des macrophages naïfs vers un phénotype anticancéreux M1, tout en inhibant l'acquisition de marqueurs pro-tumoraux de type M2.L'ensemble de nos résultats démontre le fort potentiel de nos complexes métalliques en tant que stabilisateurs de G-quadruplexes, présentant de prometteuses propriétés anticancéreuses, notamment en modulant le microenvironnement tumoral. Ces résultats ouvrent la possibilité à de nombreuses perspectives d'investigation, suggérant de nouvelles pistes thérapeutiques en cancérologie
Triple-negative breast cancer and pancreatic adenocarcinoma are associated to very low survival-rates due to their high resistance to conventional treatments, posing significant public healthiness issue. The development of new targeted therapeutic options is then crucial. G-rich sequences in nucleic acids can form non-conventional secondary structures, known as G-quadruplexes, identified in telomeric sequences and in the promoters of potent oncogenes, such as cMYC, cKIT, and BCL2. These structures play a critical role in regulating gene expression, making them as promising therapeutic targets in cancer treatment.In this study, we employed a transdisciplinary approach, integrating chemical synthesis, molecular dynamic simulations, and cellular and molecular biology, to identify novel G-quadruplex binders and stabilizers aimed at controlling cancer progression. Previous work in our laboratory demonstrated that symmetric planar metal complexes could specifically bind these structures. In that sense, we synthesized 12 new transition metal complexes of Zn2+, Ni2+, Cu2+, Pd2+ and Pt2+, from the Salphen scaffold. Their ability to selectively bind and stabilize G-quadruplexes over double-stranded DNA were confirmed. Molecular dynamic simulations revealed an unconventional binding mode involving interaction with the G-quadruplex loop.Immunofluorescence assays confirmed that the compounds enhance G-quadruplex formation, in cancer cell lines, leading to the early downregulation of several G-quadruplex-driven oncogenes, such as kRAS, RET, and cMYC. This downregulation reduced cancer cell proliferation and viability, with less effect on non-cancerous cells.Some complexes induced apoptosis in cancer cells without affecting the non-neoplastic cells, after decreased hRAS and cMYC transcript levels, while other compounds caused DNA damage in pancreatic cancer cells T3M4. Notably, Zn2+ compounds increased VEGF-A expression, enhancing its transcription. We also investigated the effects of G-quadruplex stabilization on macrophages polarization, showing that nickel compounds promoted the polarization of M0 macrophages towards the anticancer M1 phenotype, while inhibiting the acquisition of pro-tumoral M2 markers.Overall, our novel metal complexes demonstrate significant potential in stabilizing G-quadruplex and exhibit promising anticancer properties, including modulation of the tumor microenvironment. These preliminary results suggest avenues for further research, with potential implications for advancing strategies in cancer therapy

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Rost, Nathalie. "Expression et régulation du gène de la proenképhaline dans un modèle expérimental de tumeur cérébrale chez le rat." Grenoble 1, 1991. http://www.theses.fr/1991GRE10048.

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L'expression du gène précurseur de la met-enképhaline (PPE) a été analysée dans un modèle expérimental de tumeur cérébrale chez le rat, provoquée par l'injection stéréotaxique de cellules gliales malignes C6 dans le striatum. Une étude par hybridation in situ a montré une expression élevée de ce gène dans la tumeur, en l'absence in vitro, pour la lignée C6, par Yoshikawa et al. (1986). L'expression élevée du gène PPE, dans les cellules C6, ne résulterait pas d'une amplification de l'ADN, ni de l'absence d'un rétrocontrôle enképhalinergique. Le fait de trouver une expression de gènes codant pour des neuromodulateurs dans les cellules gliales normales, et malignes dans le cas présent, remet en question le concept de leur rôle exclusif de neurotransmetteur et suggère l'implication éventuelle de ce type de gènes dans la carcinogenèse. Nous avons aussi montré que, suite à une déafférentation dopaminergique, l'expression du gène PPE diminue dans la tumeur. La destruction des afférences dopaminergiques entraîne une série de changements, au niveau de plusieurs peptides striataux, variable suivant l'étendue de la lésion. La nature du/des composés responsables de la modulation de l'expression du gène PPE reste à définir. D’autre part, l'analyse de certains oncogènes, dans le modèle tumoral, a révélé l'expression des oncogènes nucléaires FOS et JUN au sein de la tumeur. Une éventuelle corrélation, entre l'expression de ces gènes codant pour des facteurs régulateurs de la transcription et l'expression du gène PPE pourrait permettre une approche originale du processus tumoral.

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Ellis, D. K. "Cellular oncogene expression during retinal transdifferentiation." Thesis, University of Nottingham, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.371121.

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Chan, Yuk Fai. "Manipulation of EWS oncogene expression using RNAi /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202005%20CHAN.

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Radhakrishnan, Vijayababu, Charles Putnam, Wenqing Qi, and Jesse Martinez. "P53 suppresses expression of the 14-3-3gamma oncogene." BioMed Central, 2011. http://hdl.handle.net/10150/610345.

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BACKGROUND:14-3-3 proteins are a family of highly conserved proteins that are involved in a wide range of cellular processes. Recent evidence indicates that some of these proteins have oncogenic activity and that they may promote tumorigenesis. We previously showed that one of the 14-3-3 family members, 14-3-3gamma, is over expressed in human lung cancers and that it can induce transformation of rodent cells in vitro.METHODS:qRTPCR and Western blot analysis were performed to examine 14-3-3gamma expression in non-small cell lung cancers (NSCLC). Gene copy number was analyzed by qPCR. P53 mutations were detected by direct sequencing and also by western blot. CHIP and yeast one hybrid assays were used to detect p53 binding to 14-3-3gamma promoter.RESULTS:Quantitative rtPCR results showed that the expression level of 14-3-3gamma was elevated in the majority of NSCLC that we examined which was also consistent with protein expression. Further analysis of the expression pattern of 14-3-3gamma in lung tumors showed a correlation with p53 mutations suggesting that p53 might suppress 14-3-3 gamma expression. Analysis of the gamma promoter sequence revealed the presence of a p53 consensus binding motif and in vitro assays demonstrated that wild-type p53 bound to this motif when activated by ionizing radiation. Deletion of the p53 binding motif eliminated p53's ability to suppress 14-3-3gamma expression.CONCLUSION:Increased expression of 14-3-3gamma in lung cancer coincides with loss of functional p53. Hence, we propose that 14-3-3gamma's oncogenic activities cooperate with loss of p53 to promote lung tumorigenesis.

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Watson, Dorothy M. A. "Cyclic nucleotide binding and oncogene expression in breast cancer." Thesis, University of Edinburgh, 1989. http://hdl.handle.net/1842/19398.

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Amouyel, Philippe. "Expression des proto-oncogenes ets dans les astrocytes et dans les tumeurs astrocytaires." Lille 2, 1988. http://www.theses.fr/1988LIL2M054.

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Ritchie, Andrew John. "Endocrinology, oncogene expression and outcome in carcinoma of the lung." Thesis, Queen's University Belfast, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357457.

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Books on the topic "Modulation of oncogene expression"

1

Darley, Richard Lawrence. Modulation of major histocompatibility antigen expression by the ras oncogene in murine fibroblast cells. [s.l.]: typescript, 1992.

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Travers, Helen. Oncogene regulation of gene expression. Manchester: University of Manchester, 1996.

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Morgan, James I. Proto-Oncogene expression in the nervous /system. Amsterdam: Published by Elsevier for the Foundation for the study of the Nervous System (FESN), 1991.

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Detta, Allah. Proliferative potential and proto-oncogene expression in human meningioma. Birmingham: Universityof Birmingham, 1993.

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Rowley, S. Nuclear oncogene expression in the prognosis of colorectal cancer. Birmingham: University of Birmingham, 1990.

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Eric, Blair G., Pringle Craig R, and Maudsley D. John, eds. Modulation of MHC antigen expression and disease. Cambridge: Cambridge University Press, 1995.

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Rottleb, Christoph. Modulation der c-myc-Expression durch exogene Stimuli. [s.l.]: [s.n.], 1991.

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Luo, Jiin-Chyuan John. Blood oncoprotein expression in colonic neoplasia. [New York]: Columbia University, School of Public Health, 1994.

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S, Denison Michael, and Helferich William, eds. Toxicant-receptor interactions: Modulation of signal transduction and gene expression. Washington, DC: Taylor & Francis, 1998.

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Palese, Peter, ed. Modulation of Host Gene Expression and Innate Immunity by Viruses. Dordrecht: Springer Netherlands, 2005. http://dx.doi.org/10.1007/1-4020-3242-0.

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Book chapters on the topic "Modulation of oncogene expression"

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Nakaishi, Hitoshi. "Functionally Distinct Oncogenes Differently Regulate Cellular Expression of Gangliosides." In Gangliosides and Modulation of Neuronal Functions, 325–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71932-5_30.

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McCarty, K. S., and K. S. McCarty. "Steroid modulation of the expression of growth factors and oncogenes in breast cancer." In Regulatory Mechanisms in Breast Cancer, 197–220. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3940-7_9.

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Robins, Roland K., Rick A. Finch, and Thomas L. Avery. "Nucleoside and Nucleotide Modulation of Oncogenic Expression: A New Approach to Cancer Chemotherapy." In Anticancer Drug Discovery and Development: Natural Products and New Molecular Models, 149–82. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2610-0_9.

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Klement, V. "Radiation-Enhanced Oncogene Expression." In Realm of Tolerance, 180–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74712-0_21.

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Höfler, H. "Oncogene and Receptor Expression." In Current Topics in Pathology, 435–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75515-6_12.

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Sasaki, Yutaka, Norio Hayashi, Masayoshi Horimoto, Toshifumi Ito, Hideyuki Fusamoto, and Takenobu Kamada. "Oncogene Expression in Liver Injury." In Liver and Environmental Xenobiotics, 151–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-12385-0_12.

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Baker, Vicki V. "Oncogene expression in cervical cancer." In Gynecologic Oncology, 43–51. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2598-1_4.

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Ichimura, Koichi, Kimiyoshi Hirakawa, Atsushi Komatsuzaki, and Yasuhito Yuasa. "Oncogene Expression in Acoustic Neurinomas." In Biological Aspects of Brain Tumors, 337–42. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68150-2_45.

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Symonds, R. P., T. Habeshaw, J. Paul, D. J. Kerr, A. Darling, R. A. Burnett, F. Sotsiou, S. Linardopoulos, and D. A. Spandidos. "Oncogene Expression and Cervical Cancer." In The Superfamily of ras-Related Genes, 277–83. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-6018-6_30.

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Murphy, Gretchen A., and Channing J. Der. "Ras-Mediated Deregulation of Gene Expression and Contribution to Oncogenesis." In Oncogene-Directed Therapies, 77–99. Totowa, NJ: Humana Press, 2003. https://doi.org/10.1007/978-1-59259-313-2_5.

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Conference papers on the topic "Modulation of oncogene expression"

1

Wang, Pengpeng, Zhan Wang, Peng You, and Yiyue Liu. "Construction of the Unified Coded Expression for Intra-Pulse Phase Modulation in Pulse Radar." In 2024 International Conference on Microwave and Millimeter Wave Technology (ICMMT), 1–3. IEEE, 2024. http://dx.doi.org/10.1109/icmmt61774.2024.10671868.

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Chakrabarti, Mrinmay, James S. Norris, Naren L. Banik, and Swapan K. Ray. "Abstract 1101: Modulation of expression of specific oncogenic and tumor suppressor microRNAs enhanced therapeutic efficacy of 4-HPR and EGCG in human malignant neuroblastoma cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1101.

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Feng, Gong, Patricia Hicks, Charles W. Prince, Candece Gladson, and Pi-Ling Chang. "OSTEOPONTIN ENHANCES PROTO-ONCOGENE (Junb) EXPRESSION IN PRENEOPLASTIC MOUSE CELLS." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.253.

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Dachineni, Rakesh, Goqiang Ai, and Jayarama B. Gunaje. "Abstract 3501: Aspirin modulates oncogene expression in hct 116 colon cancer cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3501.

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Ge, Lin, Lin Ge, Wenxia Meng, Hongmei Zhou, and Neil Bhowmick. "Abstract 1015: Head and neck cancer expression of YAP65: A novel oncogene." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1015.

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Koch, Daniel, Stacey Adams, Andrew Gentles, Benedict Anchang, Delaney Sullivan, Sylvia Plevritis, and Dean Felsher. "Abstract A48: Gene expression signatures associated with MYC oncogene addiction in lymphoma." In Abstracts: AACR Special Conference on Myc: From Biology to Therapy; January 7-10, 2015; La Jolla, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3125.myc15-a48.

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Wormser, L., A. Gaza, V. Fritz, C. Hellerbrand, AK Bosserhoff, and P. Dietrich. "Expression and function of neuroblastoma RAS viral oncogene homolog (NRAS) in hepatocellular carcinoma." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677241.

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Guerrero, Sergi, Rudolf Fehrmann, and Marcel ATM van Vugt. "Abstract 1406: Towards an RNA expression-based signature for oncogene-induced replication stress." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1406.

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Oev, M. S., E. M. Shpadaruk, and R. M. Smolyakova. "PROGNOSTIC SIGNIFICANCE OF DETERMINING THE LEVEL OF EXPRESSION OF ERCC1, TS, TP IN COLORECTAL CANCER." In SAKHAROV READINGS 2022: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2022. http://dx.doi.org/10.46646/sakh-2022-2-41-45.

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In the course of the study, it was made the analysis of the expression level in colorectal cancer of the ERCC1 oncogene in 72 patients, the TS and TP genes in 94 patients. As a result of the analysis of the obtained data, it was found that there were no statistically significant differences in the expression of the studied genes between the groups of patients who received radical treatment and combined treatment. When analyzing the prognostic significance of the studied parameters, it was found that in patients with detected progression of the disease, the predominance of hypoexpression of the ERCC1 oncogene and gene, as well as moderate expression of the TP gene, was established. The relationship between the level of expression of the studied genes and the overall survival of patients with colorectal cancer is a weak straight line (p(Spearman) <0.05).

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Benitez, Jorge A., Webster K. Cavenee, and Frank F. Furnari. "Abstract 5253: PTEN represses oncogene expression by regulating Daxx-H3.3 deposition in the chromatin." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5253.

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Reports on the topic "Modulation of oncogene expression"

1

Anderson, A., and G. E. Woloschak. Cellular oncogene expression following exposure of mice to {gamma}-rays. Office of Scientific and Technical Information (OSTI), June 1991. http://dx.doi.org/10.2172/10148918.

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Prusky, Dov, and Jeffrey Rollins. Modulation of pathogenicity of postharvest pathogens by environmental pH. United States Department of Agriculture, December 2006. http://dx.doi.org/10.32747/2006.7587237.bard.

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Until recently, environmental pH was not considered a factor in determining pathogen compatibility. Our hypothesis was that the environmental pH at the infection site, which is dynamically controlled by activities of both the host and the pathogen, regulates the expression of genes necessary for disease development in Colletotrichum gloeosporioides and Sclerotinia sclerotiorum. This form of regulation ensures that genes are expressed at optimal conditions for their encoded activities.Pectate lyase encoded by pelB, has been demonstrated to play a key role in virulence of C. gloeosporioides in avocado fruit. Polyglacturonase synergism with oxalic acid production is considered to be an essential pathogenicity determinant in the interactions of S. sclerotiorum with its numerous hosts. A common regulatory feature of these virulence and pathogenicity factors is their dependence upon environmental pH conditions within the host niche to create optimal conditions for expression and secretion. In this proposal we have examined, 1) the mechanisms employed by these fungi to establish a suitable pH environment, 2) the molecular levels at which genes and gene products are regulated in response to environmental pH, and 3) the molecular basis and functional importance of pH-responsive gene regulation during pathogenicity. The specific objectives of the proposal were: 1. Characterize the mechanism of local pH modulation and the effect of ambient pH on the expression and secretion of virulence factors. 2. Provide evidence that a conserved molecular pathway for pH-responsive gene expression exists in C. gloeosporioides by cloning a pacC gene homologue. 3. Determine the role of pacC in pathogenicity by gene disruption and activating mutations. Major conclusions 1. We determined the importance of nitrogen source and external pH in the secretion of the virulence factor pectate lyase with respect to the ambient pH transcriptional regulator pacC. It was concluded that nitrogen source availability and ambient pH are two independent signals for the transcriptional regulation of genes required for the disease process of C. gloeosporioides and possibly of other pathogens. 2. We also determined that availability of ammonia regulate independently the alkalinization process and pelB expression, pecate lyase secretion and virulence of C. gloeosporioides. 3. Gene disruption of pacC reduced virulence of C. gloeosporioides however did not reduced fully pelB expression. It was concluded that pelB expression is regulated by several factors including pH, nitrogen and carbon sources. 4. Gene disruption of pacC reduced virulence of S. slcerotiourum Creation of a dominant activating

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McGuffie, Eileen M., and Carlo V. Catapano. Development of Triplex-Forming Oligonucleotides to Inhibit Expression of the c-myc Oncogene in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada416148.

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Redmond, Sarah Beth, Rachel Tell, Derrick Coble, Carrie Mueller, Dušan Palić, Claire B. Andreasen, and Susan J. Lamont. Genetic Differences in Chicken Splenic Immune Gene Expression in Response to Dietary Immune Modulation. Ames (Iowa): Iowa State University, January 2010. http://dx.doi.org/10.31274/ans_air-180814-166.

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Dickson, Robert B. Modulation of Cyclin Expression by C-MYC in Malignant and Nonmalignant Mammary Epithelial Cells. Fort Belvoir, VA: Defense Technical Information Center, September 1995. http://dx.doi.org/10.21236/ada302398.

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Imbalzano, Anthony N. In Vivo and In Vitro Analysis of the Regulation of c-myc Proto-Oncogene Expression in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 1995. http://dx.doi.org/10.21236/ada305616.

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Woloschak, G. E., and Chin-Mei Chang-Liu. Modulation of expression of genes encoding nuclear proteins following exposure to JANUS neutrons or {gamma}-rays. Office of Scientific and Technical Information (OSTI), May 1994. http://dx.doi.org/10.2172/10148904.

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Woloschak, G. E., and Chin-Mei Chang-Liu. Modulation of expression of genes encoding nuclear proteins following exposure to JANUS neutrons or {gamma}-rays. Office of Scientific and Technical Information (OSTI), August 1994. http://dx.doi.org/10.2172/10171321.

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Broadley, Caroline, Debra A. Gonzalez, Rhada Nair, and Jeffrey M. Davidson. Canine Vocal Fold Fibroblasts in Culture: Expression of alpha-Smooth Muscle Actin and Modulation of Elastin Synthesis. Fort Belvoir, VA: Defense Technical Information Center, January 1991. http://dx.doi.org/10.21236/ada302739.

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Locy, Robert D., Hillel Fromm, Joe H. Cherry, and Narendra K. Singh. Regulation of Arabidopsis Glutamate Decarboxylase in Response to Heat Stress: Modulation of Enzyme Activity and Gene Expression. United States Department of Agriculture, January 2001. http://dx.doi.org/10.32747/2001.7575288.bard.

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Most plants accumulate the nonprotein amino acid, g-aminobutyric acid (GABA), in response to heat stress. GABA is made from glutamate in a reaction catalyzed by glutamate decarboxylase (GAD), an enzyme that has been shown by the Israeli PI to be a calmodulin (CaM) binding protein whose activity is regulated in vitro by calcium and CaM. In Arabidopsis there are at least 5 GAD genes, two isoforms of GAD, GAD1 and GAD2, are known to be expressed, both of which appear to be calmodulin-binding proteins. The role of GABA accumulation in stress tolerance remains unclear, and thus the objectives of the proposed work are intended to clarify the possible roles of GABA in stress tolerance by studying the factors which regulate the activity of GAD in vivo. Our intent was to demonstrate the factors that mediate the expression of GAD activity by analyzing the promoters of the GAD1 and GAD2 genes, to determine the role of stress induced calcium signaling in the regulation of GAD activity, to investigate the role of phosphorylation of the CaM-binding domain in the regulation of GAD activity, and to investigate whether ABA signaling could be involved in GAD regulation via the following set of original Project Objectives: 1. Construction of chimeric GAD1 and GAD2 promoter/reporter gene fusions and their utilization for determining cell-specific expression of GAD genes in Arabidopsis. 2. Utilizing transgenic plants harboring chimeric GAD1 promoter-luciferase constructs for isolating mutants in genes controlling GAD1 gene activation in response to heat shock. 3. Assess the role of Ca2+/CaM in the regulation of GAD activity in vivo in Arabidopsis. 4. Study the possible phosphorylation of GAD as a means of regulation of GAD activity. 5. Utilize ABA mutants of Arabidopsis to assess the involvement of this phytohormone in GAD activation by stress stimuli. The major conclusions of Objective 1 was that GAD1 was strongly expressed in the elongating region of the root, while GAD2 was mainly expressed along the phloem in both roots and shoots. In addition, GAD activity was found not to be transcriptionally regulated in response to heat stress. Subsequently, The Israeli side obtained a GAD1 knockout mutation, and in light of the objective 1 results it was determined that characterization of this knockout mutation would contribute more to the project than the proposed Objective 2. The major conclusion of Objective 3 is that heat-stress-induced changes in GAD activity can be explained by heat-stress-induced changes in cytosolic calcium levels. No evidence that GAD activity was transcriptionally or translationally regulated or that protein phosphorylation was involved in GAD regulation (objective 4) was obtained. Previously published data by others showing that in wheat roots ABA regulated GABA accumulation proved not to be the case in Arabidopsis (Objective 5). Consequently, we put the remaining effort in the project into the selection of mutants related to temperature adaptation and GABA utilization and attempting to characterize events resulting from GABA accumulation. A set of 3 heat sensitive mutants that appear to have GABA related mutations have been isolated and partially characterized, and a study linking GABA accumulation to growth stimulation and altered nitrate assimilation were conducted. By providing a better understanding of how GAD activity was and was not regulated in vivo, we have ruled out the use of certain genes for genetically engineering thermotolerance, and suggested other areas of endeavor related to the thrust of the project that may be more likely approaches to genetically engineering thermotolerance.

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