E1AF promotes breast cancer cell cycle progression via upregulation of Cyclin D3 transcription

Jiang, Jianhai; Wei, Yuanyan; Liu, Dan; Zhou, Jin; Shen, Jia-Lin; Chen, Xiaoning; Zhang, Si; Kong, Xue; Gu, Jianxin

doi:10.1016/j.bbrc.2007.04.043

Cited by 34 publications

(33 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PEA3 factors in mammary tumorigenesis 4 (encoding a transmembrane mucin) (Fauquette et al, 2005) and osteopontin (El-Tanani et al, 2004) in mammary cancer cell models. Furthermore, some Pea3-target genes belong to pathways implicated in proliferation or cell cycle regulation, such as Neu (Xing et al, 2000), WT1 (Discenza et al, 2004), cyclin D3 (Jiang et al, 2007) or cyclin D1 (a gene implicated in G1-S transition) for which a correlation has been established with pea3 expression in different mammary tissues and tumors (Galang et al, 2004). These findings fit well with the potential role of PEA3 members in tumorigenesis events.…”

Section: Discussionsupporting

confidence: 76%

Reduced tumorigenesis in mouse mammary cancer cells following inhibition of Pea3- or Erm-dependent transcription

Firlej

Ladam

Brysbaert

et al. 2008

Journal of Cell Science

View full text Add to dashboard Cite

Pea3 and Erm are transcription factors expressed in normal developing branching organs such as the mammary gland. Deregulation of their expression is generally associated with tumorigenesis and particularly breast cancer. By using RNA interference (RNAi) to downregulate the expression of Pea3 and/or Erm in a mammary cancer cell line, we present evidence for a role of these factors in proliferation, migration and invasion capacity of cancer cells. We have used different small interfering RNAs (siRNAs) targeting pea3 and erm transcripts in transiently or stably transfected cells, and assessed the physiological behavior of these cells in in vitro assays. We also identified an in vivo alteration of tumor progression after injection of cells that overexpress pea3 and/or erm short hairpin RNAs (shRNAs) in immunodeficient mice. Using transcriptome profiling in Pea3- or Erm-targeted cells, two largely independent gene expression programs were identified on the basis of their shared phenotypic modifications. A statistically highly significant part of both sets of target genes had previously been already associated with the cellular signaling pathways of the `proliferation, migration, invasion' class. These data provide the first evidence, by using endogenous knockdown, for pivotal and complementary roles of Pea3 and Erm transcription factors in events crucial to mammary tumorigenesis, and identify sets of downstream target genes whose expression during tumorigenesis is regulated by these transcription factors.

show abstract

Section: Discussionsupporting

confidence: 76%

Reduced tumorigenesis in mouse mammary cancer cells following inhibition of Pea3- or Erm-dependent transcription

Firlej

Ladam

Brysbaert

et al. 2008

Journal of Cell Science

View full text Add to dashboard Cite

show abstract

“…In addition, in our analysis of network 2, cell-cycle regulation was found to be altered in OV90i4 cells with cyclin B1 indicated as the core molecule. ETS transcription factors have been shown to activate the expression of cyclins D1 and D3 (40,41). We confirmed the downregulation of cyclin B1 in OV90i4 cells, suggesting that the observed decrease in cell proliferation was because of an inhibition of cell-cycle progression.…”

Section: Discussionsupporting

confidence: 74%

Analysis of Gene Expression Regulated by the ETV5 Transcription Factor in OV90 Ovarian Cancer Cells Identifies FOXM1 Overexpression in Ovarian Cancer

Llauradó

Majem²,

Castellví³

et al. 2012

Molecular Cancer Research

View full text Add to dashboard Cite

Epithelial ovarian cancer is the most lethal gynecologic malignancy and the fifth leading cause of cancer death in women in the Western world. ETS transcription factors have been implicated in the regulation of gene expression during a variety of biologic processes including cell growth and differentiation. We recently examined the role of the ETS transcription factor ETV5 in epithelial ovarian cancer and described ETV5 as being upregulated in ovarian tumor samples as compared with ovarian tissue controls. In ovarian cancer cells, we showed that ETV5 regulated the expression of cell adhesion molecules, enhancing ovarian cancer cell survival in anchorage-independent conditions and suggesting that it plays a role in ovarian cancer cell dissemination and metastasis into the peritoneal cavity. To understand the role of ETV5 transcription factor during ovarian cancer cell dissemination, we analyzed by gene expression microarray technology those genes whose expression was altered in an ovarian cancer cell line with a stable downregulation of ETV5. The analysis of the genes and signaling pathways under the control of ETV5 in OV90 cells has unraveled new signaling pathways that interact with ETV5, among them the cell-cycle progression and the TGFb signaling pathway. In addition, we found that the downregulation of ETV5 reduced the expression of the oncogenic transcription factor FOXM1. Consistently, FOXM1 was overexpressed in ovarian tumor samples, and its transcriptional levels increased with ETV5 transcription in ovarian tumor samples. Moreover, FOXM1 expression levels increased with tumor grade, suggesting a role in the progression of ovarian cancer. Mol Cancer Res; 10(7); 914-24. Ó2012 AACR. IntroductionEpithelial ovarian cancer is the most lethal gynecologic malignancy and the fifth leading cause of cancer death in women in the Western world (1). Reasons for this high lethality include the late stage at which women are diagnosed and the inherent aggressive biology of this cancer. Largely

show abstract

“…In addition to promoting cell migration and invasion, PEA3 over-expression in MDA-MB-231 breast cancer cells increased cell cycle progression, cyclin D3 transcription and in vivo tumor growth. Reciprocal PEA3 and cyclin D3 RNAi knockdown studies confirmed that the pro-proliferative function was mediated by cyclin D3 expression [88].…”

Section: Pea3mentioning

confidence: 70%

ETS Transcription Factor Expression and Conversion During Prostate and Breast Cancer Progression

Watson¹,

Turner²,

Scheiber³

et al. 2010

TOCJ

View full text Add to dashboard Cite

ETS factors are known to act as positive or negative regulators of the expression of genes including those that control response to various signaling cascades, cellular proliferation, differentiation, hematopoiesis, apoptosis, adhesion, migration, invasion and metastasis, tissue remodeling, ECM composition and angiogenesis. During cancer progression, altered ETS gene expression disrupts the regulated control of many of these biological processes. Although it was originally observed that specific ETS factors function either as positive or negative regulators of transcription, it is now evident that the same ETS factor may function in reciprocal fashions, reflecting promoter and cell context specificities. This report will present a discussion of ETS factor expression during prostate and breast cancer progression and its functional roles in epithelial cell phenotypes.The ETS genes encode transcription factors that have independent activities but are likely to be part of an integrated network. While previous studies have focused on single ETS factors in the context of specific promoters, future studies should consider the functional impact of multiple ETS present within a specific cell type. The pattern of ETS expression within a single tissue is, not surprisingly, quite complex. Multiple ETS factors may be able to regulate the same genes, albeit at different magnitude or in different directions. Furthermore, the precise balance between cancer promotion and inhibition by ETS factors, which may differentially regulate specific target genes, can thus control its progression. These concepts form the basis of the hypothesis that "Ets conversion" plays a critical role during tumor progression. Examples supporting this hypothesis will be described.Keywords: ETS, transcription, prostate cancer, breast cancer, cancer progression, biological control. ETS GENE FAMILYThe oncogene v-ets was first characterized in 1983 as part of the transforming fusion protein of an avian retrovirus, E26 (ets, E26 transforming sequence). Subsequent identification of v-ets related genes from metazoan species established the Ets family as one of the largest families of transcriptional regulators, with diverse functions and activities (for reviews, see [1][2][3][4] and references therein). To date, 27 human ETS family members have been identified (Fig. (1) and Table 1). All Ets genes retain a conserved winged helixturn-helix DNA binding domain (the ETS domain) of ~ 85 amino acids that recognizes a core GGAA/T sequence (ETS binding site, EBS). ETS proteins, with the exception of GABPα, bind DNA as monomers. The second conserved domain found in a subset of ETS genes is the pointed (PNT) domain. This 65-85 amino acid domain is found in 11 of 27 human ETS genes and has been shown to function in protein-protein interaction and oligomerization. ETS factors have been classified into 12 subgroups based upon Ets domain sequence homology: ETS, ERG, PEA3, ETV2, TCF, GABP, ELF, SPI, TEL, ERF, PDEF and ESE [2, 5] (See Table 1 for subgroup members). ...

show abstract

E1AF promotes breast cancer cell cycle progression via upregulation of Cyclin D3 transcription

Cited by 34 publications

References 28 publications

Reduced tumorigenesis in mouse mammary cancer cells following inhibition of Pea3- or Erm-dependent transcription

Reduced tumorigenesis in mouse mammary cancer cells following inhibition of Pea3- or Erm-dependent transcription

Analysis of Gene Expression Regulated by the ETV5 Transcription Factor in OV90 Ovarian Cancer Cells Identifies FOXM1 Overexpression in Ovarian Cancer

ETS Transcription Factor Expression and Conversion During Prostate and Breast Cancer Progression

Contact Info

Product

Resources

About