2010
DOI: 10.1038/nrc2681
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Emerging roles of ATF2 and the dynamic AP1 network in cancer

Abstract: Cooperation among transcription factors is central for their ability to execute specific transcriptional programmes. The AP1 complex exemplifies a network of transcription factors that function in unison under normal circumstances and during the course of tumour development and progression. This Perspective summarizes our current understanding of the changes in members of the AP1 complex and the role of ATF2 as part of this complex in tumorigenesis.Activator protein 1 (AP1) 1,2 functions in almost all areas of… Show more

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Cited by 274 publications
(294 citation statements)
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References 214 publications
(229 reference statements)
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“…c-JUN is widely expressed in skin epithelium and many other epithelial cells, but not highly in stromal cells. c-JUN is also part of the acute phase response cascade, has a role in bone formation, and has a reputation as an oncogene, and its up-regulation has been shown in various cancers (16). Although c-JUN's role in cell cycle promotion has been well established primarily in vitro (16,22), we observed a striking cell context-dependent fibrotic response in vivo.…”
Section: Discussionmentioning
confidence: 56%
See 1 more Smart Citation
“…c-JUN is widely expressed in skin epithelium and many other epithelial cells, but not highly in stromal cells. c-JUN is also part of the acute phase response cascade, has a role in bone formation, and has a reputation as an oncogene, and its up-regulation has been shown in various cancers (16). Although c-JUN's role in cell cycle promotion has been well established primarily in vitro (16,22), we observed a striking cell context-dependent fibrotic response in vivo.…”
Section: Discussionmentioning
confidence: 56%
“…Gene expression analysis suggested the dysregulation of cJUN, an AP-1 transcription factor that is a well-established regulator of critical cell biological processes and involved in cancer and other human diseases (15,16). We subsequently investigated the expression of AP-1 transcription factors in most human fibrotic diseases and found increased c-JUN expression in SMA + fibroblasts.…”
mentioning
confidence: 99%
“…23 The 11q12.2-q13.2 and 19p13.2-p13.11 segments contain several cancer-associated genes such as RIN1, FOSL1, and VEGFB (11q12.2-q13.2) and JUNB and JUND (19p13.2-p13.11) that are duplicated/rearranged and/or overexpressed in various forms of epithelial cancers. [30][31][32] Whether the 11q and 19p gains in mucoepidermoid carcinoma target any of these genes remains, however, to be shown. The most frequent copy number alterations detected in the 28 mucoepidermoid carcinomas were losses of 18q12.2-qter, 9p21.3, 6q22.1-q23.1, and 8pter-p12.1, and gains of 8q24.3, 11q12.3-q13.2, 3q26.1-q28, 19p13.2-p13.11, and 8q11.1-q12.2.…”
Section: Discussionmentioning
confidence: 99%
“…Noncanonical Wnt stimuli induce association of DVL associated activator of 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 morphogenesis (DAAM) proteins with FZD, DVL and GTP-bound Rho, which is then able to activate Rho-associated, coiled-coil containing protein kinase (ROCK) and even JNK. Although JNK is generally associated with phosphorylation and activation of c-Jun, it phosphorylates many other proteins, including activating transcription factor 2 (ATF2) and cyclic AMP response element-binding protein (CREB), which heterodimerize with c-Jun and other AP-1 family members to alter gene expression [20]. This pathway regulates cell polarity in several morphogenetic processes in vertebrates, including gastrulation, neural tube closure and orientation of stereocilia in the inner ear [19].…”
Section: Noncanonical Wnt Signalingmentioning
confidence: 99%
“…Similarly, ROR1 activates the same signaling cascade to increase CREB phosphorylation in human breast cancer cells [29]. FZDs have been found to activate a number of additional intracellular effectors, including adenylate cyclase (AC), protein kinase A (PKA) and CREB [19], p38 and ATF2 [20] and Fyn and STAT3 [21]. In addition, a new -catenin-independent aspect of Wnt signaling was recently reported in proliferating cells: Wnt signaling was found to peak at the G2/M phase of the cell cycle to produce so-called Wnt-dependent stabilization of proteins (Wnt/STOP) [30].…”
Section: Noncanonical Wnt Signalingmentioning
confidence: 99%