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c-Myc Expression
Published by Anonymous on 2007/9/30 (1682 reads)
1: Semin Oncol. 2006 Aug;33(4):498-512.


Drug targeting of the c-MYC promoter to repress gene expression via a G-quadruplex silencer element.

Hurley LH, Von Hoff DD, Siddiqui-Jain A, Yang D.

University of Arizona, College of Pharmacy, Tucson, AZ, USA. hurley@pharmacy.arizona.edu

In this review, we describe the evidence for a parallel-stranded G-quadruplex in the purine-rich strand of the nuclease hypersensitivity element III(1) (NHE III(1)) of the promoter of c-MYC upstream of the P1 and P2 promoters. This biologically relevant G-quadruplex is a mixture of four loop isomers. The folding pattern of a nuclear magnetic resonance (NMR)-derived structure for the predominant loop isomer of this G-quadruplex has been obtained. This G-quadruplex has been demonstrated to be a silencer element, and the cationic porphyrin TMPyP4 has been shown to stabilize this G-quadruplex. Furthermore, TMPyP4 has been shown to repress c-MYC expression, and this effect is mediated through the silencer element. Last, the in vivo activity of TMPyP4 in xenograph models is presented.

Publication Types:
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

PMID: 16890804 [PubMed - indexed for MEDLINE]

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2: Mol Cells. 2005 Oct 31;20(2):157-66.


c-myc expression: keep the noise down!

Chung HJ, Levens D.

Laboratory of Pathology, National Cancer Institute, Bethesda, MD 20892-1500, USA.

The c-myc proto-oncogene encodes a nuclear protein that is deregulated and/or mutated in most human cancers. Acting primarily as an activator and sometimes as a repressor, MYC protein controls the synthesis of up to 10-15% of genes. The key MYC targets contributing to oncogenesis are incompletely enumerated and it is not known whether pathology arises from the expression of physiologic targets at abnormal levels or from the pathologic response of new target genes that are not normally regulated by MYC. Regardless of which, available evidence indicates that the level of MYC expression is an important determinant of MYC biology. The c-myc promoter has architectural and functional features that contribute to uniform expression and help to prevent or mitigate conditions that might otherwise create noisy expression. Those features include the use of an expanded proximal promoter, the averaging of input from dozens of transcription factors, and real-time feedback using the supercoil-deformable Far UpStream Element (FUSE) as physical sensor of ongoing transcriptional activity, and the FUSE binding protein (FBP) as well as the FBP interacting repressor (FIR) as effectors to enforce normal transcription from the c-myc promoter.

Publication Types:
Review

PMID: 16267388 [PubMed - indexed for MEDLINE]

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3: Anticancer Res. 2003 May-Jun;23(3A):2179-83.


CRD-BP: a c-Myc mRNA stabilizing protein with an oncofetal pattern of expression.

Ioannidis P, Mahaira L, Papadopoulou A, Teixeira MR, Heim S, Andersen JA, Evangelou E, Dafni U, Pandis N, Trangas T.

Department of Genetics, St Savvas Hospital, Athens, Greece. pioannidis@ath.forthnet.gr

The Coding Region Determinant-Binding Protein (CRD-BP) is an RRM and KH-domain-containing protein that recognizes specifically at least three RNAs. It binds to one of the two c-myc mRNA instability elements, to the 5'Un Translated Region (UTR) of the leader 3 IGF-II mRNA and to the oncofetal H19 RNA. CRD-BP has been assigned a role in stabilizing c-myc mRNA by preventing its endonucleolytic cleavage and in repressing the translation of the leader 3 IGF-II mRNA, the major embryonic species of this message. CRD-BP is normally expressed only in fetal tissues. However, its expression is detected in primary tumors and transformed cell lines of different origins. The vast majority of colon (80%) and breast (60%) tumors and sarcomas (73%) express CRD-BP whereas in other tumor types, for example prostate carcinomas, its expression is rare. CRD-BP expression has also been detected in benign tumors such as breast fibroadenomas, meningiomas and other benign mesenchymal tumors, implying a role for this gene in abnormal cell proliferation. In breast carcinomas, CRD-BP expression and or gene copy number gains in the region encompassing the c-myc locus were detected in approximately 75% of tumors, implying that the deregulated expression of c-myc may be more widespread than previously believed. Infiltrated lymph nodes, corresponding to CRD-BP-positive primary tumors, were also found positive indicating that monitoring for CRD-BP could prove useful for the detection and monitoring of disseminated disease.

Publication Types:
Review

PMID: 12894594 [PubMed - indexed for MEDLINE]

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4: Cancer Lett. 2002 Jun 28;180(2):107-19.


Regulation of N-myc expression in development and disease.

Strieder V, Lutz W.

Institute of Molecular Biology and Tumor Research, Emil-Mannkopff-Strasse 2, 35033 Marburg, Germany.

Publication Types:
Review

PMID: 12175541 [PubMed - indexed for MEDLINE]

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5: Curr Top Microbiol Immunol. 1997;224:149-58.


Regulated expression and function of the c-Myc antagonist, Mad1, during a molecular switch from proliferation to differentiation.

Cultraro CM, Bino T, Segal S.

NCI-Navy Medical Oncology Branch, National Cancer Institute, NIH, Bethesds, MD, USA.

Publication Types:
Review

PMID: 9308238 [PubMed - indexed for MEDLINE]

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6: Curr Top Microbiol Immunol. 1997;224:33-46.


DNA conformation, topology, and the regulation of c-myc expression.

Levens D, Duncan RC, Tomonaga T, Michelotti GA, Collins I, Davis-Smyth T, Zheng T, Michelotti EF.

Laboratory of Pathology, National Cancer Institute, Bethesda, MD 20892, USA.

Publication Types:
Review

PMID: 9308226 [PubMed - indexed for MEDLINE]

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7: Toxicol Lett. 1993 Apr;67(1-3):161-72.


Enhanced expression of the protooncogenes c-myc and c-fos in normal and malignant renal growth.

Vamvakas S, Bittner D, Köster U.

Institut für Toxikologie, Universität Würzburg, Germany.

The protooncogenes c-myc and c-fos play an important role in growth and differentiation of renal tissue. They are highly expressed during embryogenesis in the mitotically active tubule epithelium, while in terminally differentiated tubule cells of the kidney the expression is completely shut off. Furthermore, induction of cell proliferation in cultured renal cells by addition of growth factors is preceded by enhanced expression of c-myc and c-fos. Increased expression of these protooncogenes is also obtained by treatment of kidney cells in culture with the potent nephrocarcinogen N-dimethylnitrosamine and also with the nephrotoxin and possibly nephrocarcinogen S-(1,2-dichlorovinyl)-L-cysteine. Finally, the expression of c-myc and c-fos is induced after unilateral nephrectomy during compensatory renal growth in the remaining kidney and also during regenerative cell proliferation after in vivo application of the strong nephrotoxins folic acid and mercury chloride.

Publication Types:
Review

PMID: 8451757 [PubMed - indexed for MEDLINE]

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8: Tanpakushitsu Kakusan Koso. 1993 Feb;38(2):123-8.


[Induction of apoptosis by expression of the myc family gene]

[Article in Japanese]

Kuchino Y, Asai A.

Biophysics Division, National Cancer Center Research Institute, Tokyo, Japan.

Publication Types:
Review

PMID: 8451451 [PubMed - indexed for MEDLINE]

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9: Clin Chem. 1993 Feb;39(2):353-5.


c-myc oncogene expression in estrogen-dependent and -independent breast cancer.

Shiu RP, Watson PH, Dubik D.

Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.

We demonstrate that c-myc gene expression is essential for growth of breast cancer cells. It also plays an important role in the progression of human breast cancer. c-myc gene amplification may be important for cancer cell invasion, but perhaps not essential for nodal metastasis. We also provide compelling evidence that the c-myc oncogene is an estrogen target gene in hormone-responsive breast cancer. Hormonal progression of breast cancer could be brought about by the enhanced expression of the c-myc gene, with gene amplification and enhanced c-myc mRNA stability being two major mechanisms involved.

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 8432027 [PubMed - indexed for MEDLINE]

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10: Adv Cancer Res. 1993;60:181-246.


Relationship between myc oncogene activation and MHC class I expression.

Schrier PI, Peltenburg LT.

Department of Clinical Oncology, University Hospital, Leiden, The Netherlands.

Publication Types:
Comparative Study
Research Support, Non-U.S. Gov't
Review

PMID: 8417500 [PubMed - indexed for MEDLINE]

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11: Brain Pathol. 1992 Jan;2(1):71-83.


The N-myc proto-oncogene: developmental expression and in vivo site-directed mutagenesis.

Stanton BR, Parada LF.

Molecular Embryology Section, NCI-Frederick Cancer Research and Development Center, MD 21702-1201.

The N-myc proto-oncogene is a member of the superfamily of transcription factors. In mammals, expression of this gene is predominantly restricted to the developing embryo. Specifically, the level of expression is highest in differentiating epithelial components of the embryo including those of the developing brain, kidney and lung. The observation that N-myc is expressed in differentiating but not terminally differentiated structures suggests that these genes may function in the maintenance of cells in a determined or proliferative state. Available evidence suggests that when N-myc expression is down-regulated, cells progress through differentiation and acquire their terminal phenotype. N-myc expression is also correlated with poor prognosis in a number of tumor systems. Since malignant tumors are usually poorly differentiated, this may reflect the role that N-myc plays in preventing differentiation of otherwise determined cells. In vivo site-directed mutagenesis by homologous recombination has made it possible to introduce a variety of mutations into mice. This review summarizes this technology and describes our initial results in the characterization of mice that lack a functional N-myc gene. Specifically, we have observed that in the absence of a functional N-myc gene, embryos arrest in midgestation. This body of work demonstrates that this gene is not required for normal development until the onset of organogenesis.

Publication Types:
Research Support, U.S. Gov't, P.H.S.
Review

PMID: 1341949 [PubMed - indexed for MEDLINE]

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12: J Steroid Biochem Mol Biol. 1991;40(1-3):223-30.


Estrogen induction of insulin-like growth factors and myc proto-oncogene expression in the uterus.

Murphy LJ.

Department of Internal Medicine and Physiology, University of Manitoba, Winnipeg, Canada.

In contrast to the effects observed in vivo, isolated uterine cells cultured in vitro demonstrate little proliferative response to estrogens. Estrogen induced uterine proliferation involves a carefully orchestrated, sequential activation of genes which encode a variety of biologically active molecules. These include nuclear transcription factors, growth factors and growth factor receptors. Expression of these proteins serve to amplify the effect of estrogen through cellular, autocrine and paracrine mechanisms. In this review the effects of estrogen on uterine expression of the myc family of oncogenes and the insulin-like growth factors are discussed.

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 1958525 [PubMed - indexed for MEDLINE]

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13: Ciba Found Symp. 1990;150:250-8; discussion 258-61.


Differential control of muscle-specific gene expression specified by src and myc oncogenes in myogenic cells.

Falcone G, Gauzzi MC, Tatò F, Alemà S.

Istituto di Biologia Cellulare, C.N.R., Roma, Italy.

Myogenic cells can be transformed in vitro by the introduction of several exogenous viral oncogenes. Transformed myoblasts are prevented from terminal differentiation into myotubes by the continuous expression of oncogenes such as myc and src, chosen as prototypes of nuclear and cytoplasmic oncogenes. A comparative analysis of the relationship between transformation and differentiation in myoblasts and cells belonging to other lineages has led to the proposal that terminal differentiation of myc-transformed quail myoblasts is indirectly prevented by the loss of growth control and that myc-bearing cells remain susceptible to growth regulation by interaction with adjacent normal cells. On the contrary, the src oncogene appears to affect expression of the myogenic programme via a direct mechanism, independent from abnormal growth control. There is increasing evidence for the existence of master regulatory genes that govern and influence muscle development in vivo and myogenic differentiation in vitro. Expression of cytoplasmic oncogenes such as src, ras and polyoma middle T in the mouse myogenic cell line, C2, results in inhibition of biochemical differentiation and a marked down-regulation of the MyoD1 and myogenin genes.

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 2115425 [PubMed - indexed for MEDLINE]

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14: Crit Rev Oncog. 1990;2(1):75-95.


Expression and function of myc family genes.

Zimmerman K, Alt FW.

Department of Biochemistry, Columbia University, New York, New York 10032.

The myc family of nuclear oncogenes contains three well-characterized members, c-myc, N-myc, and L-myc. These genes encode related but distinct nuclear proteins that can contribute to tumorigenic conversion both in vitro and in vivo. However, each gene displays a unique activation pattern in spontaneously arising tumors, a pattern that partially reflects the unique expression pattern of each gene during normal development. Although the specific function of myc family genes has not been determined, changes in myc gene expression accompany in vitro exposure to growth and differentiation stimuli, suggesting an important role in these cellular processes. In addition, the homologies shared among myc genes and two groups of DNA binding, transcriptional regulatory proteins suggests a role in regulating gene expression. This review describes the similar and unique properties of individual members of the myc gene family with respect to their expression and potential role during normal development and in the tumorigenic conversion process.

Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

PMID: 2091750 [PubMed - indexed for MEDLINE]

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15: Environ Health Perspect. 1989 Mar;80:161-72.


c-myc protooncogene expression in mouse erythroleukemia cells.

Lachman HM.

Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461.

Murine erythroleukemia (MEL) cells are erythroid progenitors whose programs of erythroid differentiation has been interrupted by transformation with the Friend virus complex. As a result of the ability of certain chemicals such as dimethylsulfoxide (DMSO) to induce terminal erythroid differentiation, the cells have been used as a model for understanding the molecular basis of cellular differentiation. Recent work on MEL cells as well as other differentiating systems indicates that expression of cellular protooncogenes is implicated in chemically mediated differentiation. In MEL cells the expression of the c-myc protooncogene undergoes unusual biphasic changes following inducer treatment. Levels of c-myc mRNA decrease 10- to 20-fold between 1 and 2 hr and are then reexpressed between 12 and 24 hr. These changes occur as a result of complex transcriptional and posttranscriptional regulatory events. Recent DNA transfection experiments, in which MEL cells were transfected with myc expression vectors, indicate that both the early decrease in c-myc expression and its subsequent reexpression are important events in the differentiation pathway. The work on MEL cells, as well as on other models of differentiation, is directed at understanding the molecular basis of leukemogenic transformation and cellular differentiation. The ability of c-myc, as well as other protooncogenes, to influence both of these events indicates that cellular protooncogenes play a central role in their regulation.

Publication Types:
In Vitro
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

PMID: 2647476 [PubMed - indexed for MEDLINE]

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16: In Vitro Cell Dev Biol. 1988 Feb;24(2):81-4.


Regulation of c-myc and c-fos proto-oncogene expression by animal cell growth factors.

Rollins BJ, Stiles CD.

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115.

Animal cell growth factors stimulate expression of the proto-oncogenes c-myc and c-fos. The products of these genes seem to act as intracellular mediators of the mitogenic response to growth factors. Phosphatidyl inositol breakdown products function as cytoplasmic second messengers to induce transcription of c-myc and c-fos although they may not play an exclusive role in this regard. Post-transcriptional events may contribute to the modulation of c-myc gene expression. Following induction, the c-myc and c-fos mRNAs are selectively degraded within the cell.

Publication Types:
Review

PMID: 3125143 [PubMed - indexed for MEDLINE]

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17: Exp Cell Biol. 1988;56(6):321-33.


Regulation of N-myc expression is a critical event controlling the ability of human neuroblasts to differentiate.

Thiele CJ, Israel MA.

Molecular Genetics Section, National Cancer Institute, Bethesda, Md.

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 3066661 [PubMed - indexed for MEDLINE]

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18: Bioessays. 1987 Jan;6(1):28-32.


Regulation of expression of the c-myc proto-oncogene.

Marcu KB.

Publication Types:
Review

PMID: 3551944 [PubMed - indexed for MEDLINE]

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19: Prog Clin Biol Res. 1987;239:91-112.


Expression of the c-myc proto-oncogene in prostatic tissue.

Matusik RJ, Fleming WH, Hamel A, Westenbrink TG, Hrabarchuk B, MacDonald R, Ramsey E, Gartner JG, Pettigrew NM, Johnston B, et al.

Department of Physiology, University of Manitoba, Winnipeg, Canada.

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 2443918 [PubMed - indexed for MEDLINE]

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20: Tanpakushitsu Kakusan Koso. 1986 Sep;31(11):1035-51.


[Expression of human c-myc oncogene in prokaryotic and eukaryotic cells]

[Article in Japanese]

Miyamoto C.

Publication Types:
Review

PMID: 3024232 [PubMed - indexed for MEDLINE]

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21: Annu Rev Immunol. 1986;4:317-38.


The regulation and expression of c-myc in normal and malignant cells.

Kelly K, Siebenlist U.

Publication Types:
Review

PMID: 3518746 [PubMed - indexed for MEDLINE]

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22: Nutr Rev. 1985 Aug;43(8):254-6.


Vitamin D hormone regulates myc-oncogene expression in tissue culture.

[No authors listed]

Publication Types:
Review

PMID: 2995887 [PubMed - indexed for MEDLINE]
 

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