Possible function of the c-myc product: promotion of cellular DNA replication.

Iguchi-Ariga, S. M. M.; Itani, Teru; Kiji, Y.; Ariga, Hiroyoshi

doi:10.1002/j.1460-2075.1987.tb02513.x

Cited by 150 publications

(55 citation statements)

References 47 publications

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“…Moreover, mouse 'autonomously replicating-sequence'-containing clones were selected on the basis of their affinity for the Myc protein [24]. Finally, the c-myc mRNA is also accumulated at the time of DNA synthesis in mononuclear cells stimulated with phytohemagglutinin and interleukin 2 [25].…”

Section: Discussionmentioning

confidence: 99%

Gene expression in regenerating liver in relation to cell proliferation and stress

Sobczak-Thépot

Tournier

Lotti

et al. 1989

European Journal of Biochemistry

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When hepatocyte proliferation is stimulated in the liver by partial hepatectomy, messenger RNAs coding for fibrinogen, actin, c-myc and topoisomerase I are rapidly accumulated. We distinguish an early phase of accumulation (0 -3 h after partial hepatectomy) which is also observed after a sham operation for the four genes, and during inflammation produced by Freund's adjuvant in the case of fibrinogen and c-myc genes. The hepatic response to inflammation appears therefore to mimic events characteristic of the GO/Gl transition, such as the accumulation of the c-myc mRNA. The late phase of mRNA accumulation (beyond 3 h after partial hepatectomy) is typical of liver regeneration. The level of c-myc mRNA is transiently increased (20-fold over normal) 20 h after partial hepatectomy, that is, at the time of DNA synthesis. Topoisomerase-I mRNA level increases between 3 and 24 h after partial hepatectomy (5 -10-fold over normal). These results suggest that accumulation of c-myc and topoisomerase-I mRNAs is associated with DNA replication in regenerating liver.Sequential activation of growth-related genes has been described in a number of proliferating cells, especially in mitogen-stimulated fibroblasts [l] and lymphocytes [2]. These genes probably characterize the sequential steps in the GO/Gl transition.Regenerating liver provides normal, in-vivo-proliferating hepatocytes. Although this system is complex and is under the control of a number of mitogenic stimuli [3,4], the sequence of mRNA induction in regenerating liver follows the same kinetics as in cultured fibroblasts: a transient increase in the level of the c$os mRNA (30 min after partial hepatectomy) [5] is followed by an increase in c-myc mRNA (3 h after partial hepatectomy) [6] and Ha-ras mRNA (24 h after partial hepatectomy) [7]. The accumulation of c--0.7 mRNA has also been reproduced in cultures of primary rat hepatocytes stimulated by EGF [5]. Other genes are activated in regenerating rat liver during the progression towards the S phase; namely the genes coding for actin and tubulin (8 h after partial hepatectomy) [8], p53 (8 h after partial hepatectomy) [9] and Kiras (> 12 h after partial hepatectomy) [lo].In a previous work, we have found that a and P-fibrinogen mRNAs were accumulated beyond 8 h after partial hepatectomy [l 11. Here, we describe that a transient increase in the level of fibrinogen mRNAs is detectable as soon as 15 min after partial hepatectomy. In addition, the same feature is shared by the actin mRNA, the level of which is also increased 15 min after partial hepatectomy. Moreover, this early activation was also found to take place after a sham operation. This result raised two questions : (a) Are proliferation-specific mRNAs also accumulated after a sham operation or, more generally, after stress? (b) Is it possible to distinguish between the events which are specific for cell proliferation and those which are related to stress? We have tried to answer these questions by studying, in the course of liver regeneration, the accumulation of ...

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Section: Discussionmentioning

confidence: 99%

Gene expression in regenerating liver in relation to cell proliferation and stress

Sobczak-Thépot

Tournier

Lotti

et al. 1989

European Journal of Biochemistry

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“…Its proposed role as a transcription factor by modulating the expression of several identi®ed target genes su ers from modest speci®city and intensity of induction (Grandori et al, 1996;Packham and Cleveland, 1997;Sakamuro et al, 1995). Similarly, the possible role of c-Myc in activating DNA origins of replication is highly controversial (Iguchi-Ariga et al, 1987;LuÈ scher and Eisenman, 1990). However contentious the debate, an underlying commonality in the proposed mechanisms is the ability of Myc to alter chromatin structure.…”

Section: Previous Work With Myc-er Cells Demonstrated That Myc-inducementioning

confidence: 99%

Quiescence versus apoptosis: Myc abundance determines pathway of exit from the cell cycle

et al. 1998

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“…[2][3][4] c-Myc is known to regulate transcription of more than 50% of genes present in cells, including genes related to metabolism, ribosomal synthesis and progression of the cell cycle, thereby leading to increase of cell mass. [3][4][5] We have found for the first time that c-Myc is a factor that regulates initiation of DNA replication 6) and that c-Myc binds to one of the replication origins located at the region upstream of the c-myc gene, which also acts as a transcriptional enhancer, in association with origin recognition complex (ORC) and sequence-specific DNA-binding protein Myc Single-Strand binding Proteins (MSSP), one of the c-Myc-binding proteins we identified. [7][8][9][10][11] This case is also true for the replication origin/enhancer in the heat shock protein 70 gene to which c-Myc/NF-Y binds, 12) giving rise to the idea of a concerted mechanism of DNA replication and transcription.…”

Section: Function Of C-myc and Identification Of C-myc-binding Proteinsmentioning

confidence: 99%

Common Mechanisms of Onset of Cancer and Neurodegenerative Diseases

Ariga

2015

Biological & Pharmaceutical Bulletin

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Onset of cancer and neurodegenerative disease occurs by abnormal cell growth and neuronal cell death, respectively, and the number of patients with both diseases has been increasing in parallel with an increase in mean lifetime, especially in developed countries. Although both diseases are sporadic, about 10% of the diseases are genetically inherited, and analyses of such familial forms of gene products have contributed to an understanding of the molecular mechanisms underlying the onset and pathogenesis of these diseases. I have been working on c-myc, a protooncogene, for a long time and identified various c-Myc-binding proteins that play roles in c-Myc-derived tumorigenesis. Among these proteins, some proteins have been found to be also responsible for the onset of neurodegenerative diseases, including Parkinson's disease, retinitis pigmentosa and cerebellar atrophy. In this review, I summarize our findings indicating the common mechanisms of onset between cancer and neurodegenerative diseases, with a focus on genes such as DJ-1 and Myc-Modulator 1 (MM-1) and signaling pathways that contribute to the onset and pathogenesis of cancer and neurodegenerative diseases.

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Possible function of the c-myc product: promotion of cellular DNA replication.

Cited by 150 publications

References 47 publications

Gene expression in regenerating liver in relation to cell proliferation and stress

Gene expression in regenerating liver in relation to cell proliferation and stress

Quiescence versus apoptosis: Myc abundance determines pathway of exit from the cell cycle

Common Mechanisms of Onset of Cancer and Neurodegenerative Diseases

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