<i>Myc</i> oncogenes: the enigmatic family

Ryan, Kevin M.; Birnie, G.D.

doi:10.1042/bj3140713

Cited by 155 publications

(107 citation statements)

References 105 publications

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“…In cell culture, c-Myc2 is synthesized in growing cells, while expression of c-Myc1 increases dramatically, to a level equal to or greater than that of c-Myc2 as the cells approach high density (Ryan & Birnie 1996). These observations lead to an hypothesis that in this context c-Myc1 may act as a growth inhibitor, expression of which may be triggered by contact-inhibition (Ryan & Birnie 1996). Regulation of c-MycS is much less known, relative to c-Myc1 and c-Myc2.…”

Section: The C-myc Gene and C-myc Proteinsmentioning

confidence: 99%

c-Myc in breast cancer.

Liao¹,

Dickson²

2000

Endocrine-Related Cancer

314

271

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Ever since Bishop and his co-workers discovered the c-myc gene in the late 1970s (Bishop 1982), voluminous literature has documented its central role in proliferation and malignant transformation of human and animal cells (Amati et al. 1998, Bouchard et al. 1998, Dang et al. 1999). Most, if not all, types of human malignancy have been reported to have amplification and/or overexpression of this gene, although the frequency of these alterations varies greatly among different reports (Nesbit et al. 1999). In 1992, researchers started to realize that aberrant expression of c-myc could cause apoptosis (Evan et al. 1992, Shi et al. 1992), although the phenomenon had actually been observed much earlier (Wurm et al. 1986). Studies in recent years have further shown that the c-myc gene regulates growth, both in the sense of cell size and in the context of tissue differentiation (Gandarillas & Watt 1997, Iritani & Eisenman 1999, Johnston et al. 1999, Schmidt 1999, Schuhmacher et al. 1999). Thus, it is now known that the c-myc gene participates in most aspects of cellular function, including replication, growth, metabolism, differentiation, and apoptosis (Packham & Cleveland 1995, Hoffman & Liebermann 1998, Dang 1999, Dang et al. 1999, Elend & Eilers 1999, Prendergast 1999). How the c-Myc protein may be specifically directed to perform one, but not the others, of these functions is still obscure, despite the fact that the relevant literature has been accumulating at a fast pace in the past two decades. This review focuses on the profound roles of c-Myc in breast cancer and in the actions of the hormones that are eitologically related to breast cancer.

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Section: The C-myc Gene and C-myc Proteinsmentioning

confidence: 99%

c-Myc in breast cancer.

Liao¹,

Dickson²

2000

Endocrine-Related Cancer

314

271

View full text Add to dashboard Cite

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“…Induced expression of c-Myc, a helixloop-helix transcription factor, is of great importance in controlling cell growth and vitality (63), and is commonly amplified in many human tumors (64). Involvement of c-Myc in colon cancer development downstream of the Wnt/APC/␤-catenin signaling pathway has been documented (65,66).…”

Section: Mpges-1 and Tumorigenesismentioning

confidence: 99%

Potential Role of Microsomal Prostaglandin E Synthase-1 in Tumorigenesis

Kamei

Murakami

Nakatani

et al. 2003

Journal of Biological Chemistry

181

168

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Microsomal prostaglandin E 2 synthase-1 (mPGES-1) is a stimulus-inducible enzyme that functions downstream of cyclooxygenase (COX)-2 in the PGE 2 -biosynthetic pathway. Given the accumulating evidence that COX-2-derived PGE 2 participates in the development of various tumors, including colorectal cancer, we herein examined the potential involvement of mPGES-1 in tumorigenesis. Immunohistochemical analyses demonstrated the expression of both COX-2 and mPGES-1 in human colon cancer tissues. HCA-7, a human colorectal adenocarcinoma cell line that displays COX-2-and PGE 2 -dependent proliferation, expressed both COX-2 and mPGES-1 constitutively. Treatment of HCA-7 cells with an mPGES-1 inhibitor or antisense oligonucleotide attenuated, whereas overexpression of mPGES-1 accelerated, PGE 2 production and cell proliferation. Moreover, cotransfection of COX-2 and mPGES-1 into HEK293 cells resulted in cellular transformation manifested by colony formation in soft agar culture and tumor formation when implanted subcutaneously into nude mice. cDNA array analyses revealed that this mPGES-1-directed cellular transformation was accompanied by changes in the expression of a variety of genes related to proliferation, morphology, adhesion, and the cell cycle. These results collectively suggest that aberrant expression of mPGES-1 in combination with COX-2 can contribute to tumorigenesis.Clinical, genetic, and biochemical evidence has suggested that prostaglandin (PG) 1 E 2 produced via the cyclooxygenase (COX)-2-dependent pathway plays a crucial role in the development of colorectal cancer and possibly other cancers (1). Non-steroidal anti-inflammatory drugs, which inhibit COX-2, reduce the incidence of colorectal cancer (2-4). The major prostanoid produced by several types of cancer is PGE 2 , which is produced by three biosynthetic reactions involving phospholipase A 2 (PLA 2 ), COX, and terminal PGE 2 synthase (PGES). PGE 2 promotes survival and motility of colon cancer cells in vitro and promotes tumorigenesis and angiogenesis in vivo (5-7). High levels of constitutive expression of COX-2 have been found in various cancer cells and tissues (8,9), and studies employing overexpression, antisense suppression, and specific inhibitors of COX-2 have demonstrated that COX-2 contributes to the progression of several types of cancer (10 -12).More direct evidence for the role of COX-2 and its product PGE 2 in colorectal tumorigenesis has been provided by gene targeting studies. Gene disruption of either COX-2 (13) or the PGE receptor EP2 (14) results in reduction of the number and size of intestinal polyps in Apc mutant mice, a model for human familial adenomatous polyposis. In another model, disruption of the genes for the PGE receptors EP1 (15) or EP4 (16) suppresses the development of colorectal cancer induced by carcinogen. Moreover, gene knockout of cytosolic PLA 2 ␣ (cPLA 2 ␣), which supplies the substrate arachidonic acid to COX-2, also leads to reduced polyposis in Apc mutant mice (17,18).PGES catalyzes the conversion of PGH 2 ...

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“…[1][2][3][4][5][6]. c-Myc complexed with Max recognizes the E-box sequence in the target genes to be transactivated, and many candidate genes for c-Myc-Max have been reported.…”

mentioning

confidence: 99%