Relevant bibliographies by topics / Growth-regulated oncogene

Academic literature on the topic 'Growth-regulated oncogene'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Growth-regulated oncogene"

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Chernov, A. N. "The impact of the nerve growth factor on the number of MYCC, MYCN oncogene copies in human medulloblastoma cells." Malignant tumours 9, no. 1 (April 10, 2019): 22–28. http://dx.doi.org/10.18027/2224-5057-2019-9-1-22-28.

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Introduction: The search for new molecular targets for chemotherapy of malignancies, particularly pediatric brain tumors, is a relevant issue of modern oncology. MYC expression and amplification is often observed in brain tumors, which is an unfavorable prognostic factor. Many oncogenic processes are regulated by some growth factors including the nerve growth factor (NGF).Purpose: To study the changes in the number of MYCCand MYCN‑gene copies in MB cells exposed to the NGF.Material and methods: The impact of the NGF on the number of MYCC‑, MYCN oncogene copies in the primary human medulloblastoma cell culture was assessed using the method of fluorescence in situ hybridization.Results: Exposure to the NGF was shown to decrease the number of MB cells containing 6, 8 copies of MYCN oncogenes and 3, 8 copies of MYCC oncogene. The NGF was also shown to increase the number of tumor cells that contain a double set of copies of both oncogenes. There was a statistically significant (p<0.0001) negative correlation (r=–0.65) between the average number of MYCC oncogene copies and the NGF cytotoxicity index.Conclusion: The increased number of oncogene copies reduces the susceptibility of MB cells to the growth factor.
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Karpatkin, Simon. "Growth regulated oncogene is pivotal in thrombin-induced angiogenesis." Thrombosis Research 120 (January 2007): S71—S74. http://dx.doi.org/10.1016/s0049-3848(07)70133-0.

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Caunt, Maresa, Liang Hu, Thomas Tang, Peter C. Brooks, Sherif Ibrahim, and Simon Karpatkin. "Growth-Regulated Oncogene Is Pivotal in Thrombin-Induced Angiogenesis." Cancer Research 66, no. 8 (April 15, 2006): 4125–32. http://dx.doi.org/10.1158/0008-5472.can-05-2570.

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4

Lee, Wei-Ping, Yong Liao, Dan Robinson, Hsing-Jien Kung, Edison T. Liu, and Mien-Chie Hung. "Axl-Gas6 Interaction Counteracts E1A-Mediated Cell Growth Suppression and Proapoptotic Activity." Molecular and Cellular Biology 19, no. 12 (December 1, 1999): 8075–82. http://dx.doi.org/10.1128/mcb.19.12.8075.

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ABSTRACT The adenovirus type 5 early region 1A gene (E1A) has previously been known as an immortalization oncogene because E1A is required for transforming oncogenes, such as ras andE1B, to transform cells in primary cultures. However, E1A has also been shown to downregulate the overexpression of theHer-2/neu oncogene, resulting in suppression of transformation and tumorigenesis induced by that oncogene. In addition, E1A is able to promote apoptosis induced by anticancer drugs, irradiation, and serum deprivation. Many tyrosine kinases, such as the epidermal growth factor receptor, Her-2/Neu, Src, and Axl, are known to play a role in oncogenic signals in transformed cells. To study the mechanism underlying the E1A-mediated tumor-suppressing function, we exploited a modified tyrosine kinase profile assay (D. Robinson, F. Lee, T. Pretlow, and H.-J. Kung, Proc. Natl. Acad. Sci. USA 93:5958–5962, 1996) to identify potential tyrosine kinases regulated by E1A. Reverse transcription (RT)-PCR products were synthesized with two degenerate primers derived from the conserved motifs of various tyrosine kinases. A tyrosine kinase downregulated by E1A was identified by analyzing the AluI-digested RT-PCR products. We isolated the DNA fragment of interest and found that E1A negatively regulated the expression of the transforming receptor tyrosine kinase Axl at the transcriptional level. To study whether downregulation of the Axl receptor is involved in E1A-mediated growth suppression, we transfectedaxl cDNA into E1A-expressing cells (ip1-E1A) to establish cells that overexpressed Axl. The Axl ligand Gas6 triggered a greater mitogenic effect in these ip1-E1A-Axl cells than in ip1-E1A control cells and protected the Axl-expressing cells from serum deprivation-induced apoptosis. These results indicate that downregulation of the Axl receptor by E1A is involved in E1A-mediated growth suppression and E1A-induced apoptosis and thereby contributes to E1A’s antitumor activities.
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Zhang, Xin, Tao Zhu, Yong Chen, Hichem C. Mertani, Kok-Onn Lee, and Peter E. Lobie. "Human Growth Hormone-regulated HOXA1 Is a Human Mammary Epithelial Oncogene." Journal of Biological Chemistry 278, no. 9 (December 13, 2002): 7580–90. http://dx.doi.org/10.1074/jbc.m212050200.

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Caunt, Maresa, Liang Hu, Thomas Tang, Peter C. Brooks, and Simon Karpatkin. "Growth Regulated Oncogene (GRO-α) Is Pivotal in Thrombin-Induced Angiogenesis." Blood 106, no. 11 (November 16, 2005): 530. http://dx.doi.org/10.1182/blood.v106.11.530.530.

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Abstract The mechanism of thrombin-induced angiogenesis is poorly understood. Using a gene chip array to investigate the pro-malignant phenotype of thrombin-stimulated cells we observed that thrombin (0.5–1 u/ml/24 hr) upregulates GRO-α 168 fold in an undifferentiated mouse cell line (UMCL). Thrombin-induced GRO-α upregulation was also observed in several tumor cell lines [murine B16F10 melanoma and 4T1 breast CA, human DU145 and PC3 prostate CA, human MCF7 breast CA, as well as human umbilical vein (HUVEC) and brain microvascular endothelial cells] by mRNA and protein analysis. Thrombin enhanced the secretion of GRO-α from PC3 and MCF7 cells 25–64 fold at 24 hrs. GRO-α is a CXC chemokine oncogene that binds to a seven transmembrane receptor, CXCR2 and enhances growth, chemotaxis and metastasis of several tumor cell lines. GRO-α induced metastasis is associated with increased angiogenesis. To obtain a better understanding of neoangiogenesis mechanisms involved in the thrombin-stimulated malignant phenotype we examined the effect of anti-GRO-α Ab on thrombin-induced angiogenesis in the CAM assay at 72 hrs. GRO-α (5ug/egg/day) enhanced angiogenesis 2.2 fold (n=19, p=0.005), providing direct evidence for GRO-α as an angiogenic growth factor. Thrombin also enhanced angiogenesis 2.7 fold (n=9, p=0.01), however, anti-GRO-α Ab inhibited thrombin-induced angiogenesis to basal control levels whereas IgG control Ab had no effect (n=9). Similar results were obtained with an endothelial (HUVEC) cord formation assay in matrigel. Thrombin-induced cord formation increased 1.5 fold (n=20, p<0.0001) at 24 hrs which was inhibited by anti-GRO-α Ab to basal control levels (n=6, p<0.01). We next examined the relationship between thrombin and GRO-α on the upregulation of various vascular growth factors and receptor genes in HUVEC at 24 hrs. Thrombin as well as its PAR-1 receptor activation peptide (TRAP, 100 uM) as well as GRO-α (3 ug/ml) all markedly upregulated (>2-4 fold) KDR, Ang-2, MMP-1, MMP-2, CXCR2 and CD31 (angiogenesis marker) protein compared to control cells (n=3). Similar upregulation of GRO-α was also noted in tumor cells (PC3, B16F10 and 4T1 cells) (n=3). All of the thrombin/TRAP gene upregulations were completely inhibited by anti-GRO-α Ab and unaffected by irrelevant Ab-treated cells (n=3). bFGF and VEGF had no effect on upregulation of GRO-α (immunoblot) yet they upregulated other vascular growth factors, demonstrating specificity for thrombin. Similar inhibition of thrombin upregulation of vascular growth factors was noted in siRNA GRO-α knock down (KD) HUVEC as well as 4T1 and B16F10 cells. In vivo tumor growth studies in wild-type mice injected with subcutaneous GRO-α KD 4T1 cells revealed 2-4 fold impaired tumor growth, spontaneous metastasis and angiogenesis which was not affected by endogenous thrombin (hirudin treatment). Thus thrombin-induced angiogenesis requires the upregulation of GRO-α. Thrombin upregulation of GRO-α in tumor cells as well as endothelial cells, contributes to tumor angiogenesis.
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Nandi, Sisir, and Manish C. Bagchi. "Exploring CDKs, Ras-ERK, and PI3K-Aktin Abnormal Signaling and Cancer." Journal of Cancer Research Updates 11 (October 27, 2022): 63–69. http://dx.doi.org/10.30683/1929-2279.2022.11.09.

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Cancer or malignancy can be defined as abnormal growth and cell division. Malignancies spread, through metastasis invasion, or implantation into distant sites by which cancer cells can move through the bloodstream or lymphatic system to distant locations. The body cells follow mitotic cell division process. Normal cell division occurs through the normal signal transduction through proto-oncogenes responsible for the cell proliferation and differentiation. Mutation of these proto-oncogene leads to oncogene which can modify the gene expression and function through abnormal signal transduction, making uncontrolled growth of cells. The mitotic cell cycle is regulated by the signal transduction through the cyclin dependent kinases (CDKs), Ras-ERK and PI3K-Akt.Abnormal signaling occurs through the mutation of these genes leading to the cancer. The present review shortly reported the role of these proteins in abnormal signal transduction and cancer.
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Robinson, Shenandoah, Marie Tani, Robert M. Strieter, Richard M. Ransohoff, and Robert H. Miller. "The Chemokine Growth-Regulated Oncogene-α Promotes Spinal Cord Oligodendrocyte Precursor Proliferation." Journal of Neuroscience 18, no. 24 (December 15, 1998): 10457–63. http://dx.doi.org/10.1523/jneurosci.18-24-10457.1998.

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Lane, Brian R., Jianguo Liu, Paul J. Bock, Dominique Schols, Michael J. Coffey, Robert M. Strieter, Peter J. Polverini, and David M. Markovitz. "Interleukin-8 and Growth-Regulated Oncogene Alpha Mediate Angiogenesis in Kaposi's Sarcoma." Journal of Virology 76, no. 22 (November 15, 2002): 11570–83. http://dx.doi.org/10.1128/jvi.76.22.11570-11583.2002.

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ABSTRACT The development of the complex neoplasm Kaposi's sarcoma is dependent on infection with the Kaposi's sarcoma-associated herpesvirus (KSHV) and appears to be greatly enhanced by cytokines and human immunodeficiency virus type 1 (HIV-1) Tat. Interleukin-8 (IL-8) and growth-regulated oncogene alpha (GRO-α) are chemokines involved in chemoattraction, neovascularization, and stimulation of HIV-1 replication. We have previously demonstrated that production of GRO-α is stimulated by exposure of monocyte-derived macrophages (MDM) to HIV-1. Here we show that exposure of MDM to HIV-1, viral Tat, or viral gp120 leads to a substantial increase in IL-8 production. We also demonstrate that IL-8 and GRO-α are induced by KSHV infection of endothelial cells and are crucial to the angiogenic phenotype developed by KSHV-infected endothelial cells in cell culture and upon implantation into SCID mice. Thus, the three known etiological factors in Kaposi's sarcoma pathogenesis—KSHV, HIV-1 Tat, and cellular growth factors—might be linked, in part, through induction of IL-8 and GRO-α.
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Nasu, K. "Expression and regulation of growth-regulated oncogene alpha in human endometrial stromal cells." Molecular Human Reproduction 7, no. 8 (August 1, 2001): 741–46. http://dx.doi.org/10.1093/molehr/7.8.741.

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Dissertations / Theses on the topic "Growth-regulated oncogene"

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Mei-YinYe and 葉美吟. "Role of growth-regulated oncogene-α from oral pre-cancer associated fibroblasts in oral cancer progression." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/b5p3yg.

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Doyle, Catherine Jane. "Azithromycin suppresses P. gingivalis LPS induced pro-inflammatory cytokine and chemokine production (IL-6, IL-8, MCP-1 & GRO) by human gingival fibroblasts in vitro." Thesis, 2014. http://hdl.handle.net/2440/84847.

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Azithromycin is a macrolide antibiotic that is well known for its antibacterial properties, as well as possessing potential anti-inflammatory and immune modulating effects. This antibiotic has therefore been widely used in medicine for treating conditions ranging from inflammatory pulmonary diseases to dermatologic skin conditions. It has also been shown to be an effective antibiotic against most common periodontal pathogens and is used as an adjunct to treat periodontitis, a condition with bacterial aetiology and an inflammatory pathogenesis. Furthermore, periodontal case studies report regeneration of alveolar bone accompanied by significant reductions in inflammation have been achieved with azithromycin. The mechanisms however, by which these are achieved in the periodontium are largely unknown. This study aimed to determine the potential anti-inflammatory effect of azithromycin on cytokine and chemokine production by healthy human gingival fibroblasts (HGFs) that were stimulated by Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS). HGFs were isolated from healthy gingiva collected from three donors. The effects of azithromycin at concentrations ranging from 0.1 to 10 μg/mL were tested. Cytokine and chemokine protein levels were assessed using the Luminex® multiplex immunoassay. P. gingivalis LPS induced cytokine/chemokine (IL-6, IL-8, MCP-1 and GRO) protein production in HGFs was suppressed by azithromycin at all concentrations tested, and in all three donors. Suppression by azithromycin of IL-6, IL-8, MCP-1 and GRO P. gingivalis LPS protein induction in HGF was statistically significant when all donor results were collated (p<0.05). This study demonstrates that azithromycin suppresses P. gingivalis LPS induced cytokine/chemokine protein production in HGFs, which may explain some of the clinical benefits observed with the adjunctive use of azithromycin in the treatment of periodontitis.
Thesis (D.Clin.Dent.) -- University of Adelaide, School of Dentistry, 2014
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Books on the topic "Growth-regulated oncogene"

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White, Stacey. Induction of chemotaxis on non IL-2 stimulated human peripheral blood natural killer cells by interleukin-15 and growth regulated oncogene (A novel finding). Sudbury, Ont: Laurentian University, Department of Biology, 1997.

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Book chapters on the topic "Growth-regulated oncogene"

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Song, Jie, and Maréne Landström. "Lys63-Linked Polyubiquitination of Transforming Growth Factor β Type I Receptor (TβRI) Specifies Oncogenic Signaling." In Ubiquitin - Proteasome Pathway. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.93065.

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Transforming growth factor β (TGFβ) is a multifunctional cytokine with potent regulatory effects on cell fate during embryogenesis, in the normal adult organism, and in cancer cells. In normal cells, the signal from the TGFβ ligand is transduced from the extracellular space to the cell nucleus by transmembrane serine–threonine kinase receptors in a highly specific manner. The dimeric ligand binding to the TGFβ Type II receptor (TβRII) initiates the signal and then recruits the TGFβ Type I receptor (TβRI) into the complex, which activates TβRI. This causes phosphorylation of receptor-activated Smad proteins Smad2 and Smad3 and promotes their nuclear translocation and transcriptional activity in complex with context-dependent transcription factors. In several of our most common forms of cancer, this pathway is instead regulated by polyubiquitination of TβRI by the E3 ubiquitin ligase TRAF6, which is associated with TβRI. The activation of TRAF6 promotes the proteolytic cleavage of TβRI, liberating its intracellular domain (TβRI-ICD). TβRI-ICD enters the cancer cell nucleus in a manner dependent on the endosomal adaptor proteins APPL1/APPL2. Nuclear TβRI-ICD promotes invasion by cancer cells and is recognized as acting distinctly and differently from the canonical TGFβ-Smad signaling pathway occurring in normal cells.
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Reports on the topic "Growth-regulated oncogene"

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Pantschenko, Alexander G. The Role of Growth-Regulated Oncogene (GRO) Proteins in Human Breast Cancer Growth. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada395922.

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