Regulation of FGF receptor-2 expression by transcription factor E2F-1

Tashiro, Etsu; Minato, Yusuke; Maruki, Hiroko; Asagiri, Masataka; Imoto, Masaya

doi:10.1038/sj.onc.1206636

Cited by 37 publications

(28 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, the birth size would determine the number of growth receptors present and the initial growth rate during the sizer phase. A recent experiment (Tashiro et al, 2003) showed that FGF receptor-2 transcription was constant during early portions of the cell cycle where cell growth would normally occur but was induced in the mid-to-late G1 phase of the cell cycle in serum-starved mouse NIH3T3 cells. Other growth signaling proteins that localize to the cell membrane, such as PI 3-kinase and PDK1, are also candidate proteins.…”

Section: Discussionmentioning

confidence: 99%

Coordination of cell growth and cell division: a mathematical modeling study

Weiss

MacLellan

2004

Journal of Cell Science

View full text Add to dashboard Cite

Although there is general agreement that cell growth and division are functionally coordinated, the mechanisms that link the two processes are poorly understood. In this study, we have developed a mathematical model based on current biological concepts of the signaling transduction pathways involved in cell growth, which predicts that cell growth rate is proportional to cell surface area at birth. To investigate the relationship between growth control and cell division, we then applied our mathematical model to three classic experiments measuring cycle time versus cell birth size in fission yeast and Xenopus laevis, and the cell cycle delay in mammalian cells after serum withdrawal. When coupled to a cell cycle exhibiting `sizer' and `timer' phases, we show that a simple model in which growth rate is proportional to the cell surface area immediately after division reproduces the experimental observations including the relationship between cycle time and birth size in fission yeast and Xenopus laevis. The model also accounts for the cell cycle delay seen in restriction point experiments performed in HeLa cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Coordination of cell growth and cell division: a mathematical modeling study

Weiss

MacLellan

2004

Journal of Cell Science

View full text Add to dashboard Cite

show abstract

“…Recently, FGFR1 amplification and overexpression has been revealed as key in resistance to adjuvant tamoxifen (Turner et al, 2010b), and integrative profiling has shown FGFR2 overexpression to be a promising therapeutic target in triple-negative breast cancer (Turner et al, 2010a). Accordingly, the expression of FGFR1 and FGFR2 is partially regulated by E2F1 (Tashiro et al, 2003;Kanai et al, 2009). Furthermore, targeting FGFR-mediated signaling that acts in an autocrine manner in a subset of breast cancers of poor prognosis has been shown to impair tumor outgrowth and metastasis (Dey et al, 2010).…”

Section: Effect Of 17be2 Through Eramentioning

confidence: 99%

Biological reprogramming in acquired resistance to endocrine therapy of breast cancer

et al. 2010

View full text Add to dashboard Cite

Endocrine therapies targeting the proliferative effect of 17b-estradiol through estrogen receptor a (ERa) are the most effective systemic treatment of ERa-positive breast cancer. However, most breast tumors initially responsive to these therapies develop resistance through molecular mechanisms that are not yet fully understood. The longterm estrogen-deprived (LTED) MCF7 cell model has been proposed to recapitulate acquired resistance to aromatase inhibitors in postmenopausal women. To elucidate this resistance, genomic, transcriptomic and molecular data were integrated into the time course of MCF7-LTED adaptation. Dynamic and widespread genomic changes were observed, including amplification of the ESR1 locus consequently linked to an increase in ERa. Dynamic transcriptomic profiles were also observed that correlated significantly with genomic changes and were predicted to be influenced by transcription factors known to be involved in acquired resistance or cell proliferation (for example, interferon regulatory transcription factor 1 and E2F1, respectively) but, notably, not by canonical ERa transcriptional function. Consistently, at the molecular level, activation of growth factor signaling pathways by EGFR/ERBB/AKT and a switch from phospho-Ser118 (pS118)-to pS167-ERa were observed during MCF7-LTED adaptation. Evaluation of relevant clinical settings identified significant associations between MCF7-LTED and breast tumor transcriptome profiles that characterize ERa-negative status, early response to letrozole and tamoxifen, and recurrence after tamoxifen treatment. In accordance with these profiles, MCF7-LTED cells showed increased sensitivity to inhibition of FGFR-mediated signaling with PD173074. This study provides mechanistic insight into acquired resistance to endocrine therapies of breast cancer and highlights a potential therapeutic strategy.

show abstract

“…An increase of the cyclin D1 level determines an accumulation of the hyperphosphorylated form of pRb, leading to pRb inactivation and therefore to the release of a transcriptionally active E2F-1 factor, responsible for the activation of the fibroblast growth factor receptor 1 (FGFR-1) promoter. E2F-2 and E2F-3, the other two members of the E2F family regulated by pRb, can also increase FGFR-1 promoter activity, whereas E2F-4 and E2F-5, and consequently their negative regulators pRb2/p130 and p107, do not seem to be involved in the modulation of FGFR-1 expression (Tashiro et al, 2003).…”

Section: Involvement Of Rb Family In Angiogenesis C Gabellini Et Almentioning

confidence: 99%

Involvement of RB gene family in tumor angiogenesis

Gabellini¹,

Bufalo²,

Zupi³

2006

Oncogene

View full text Add to dashboard Cite

Angiogenesis, the development of new blood vessels from pre-existing vessels, represents a fundamental step in tumor progression and metastatization. The induction of vasculature is required for growth of the tumor mass, to ensure an adequate supply of oxygen and metabolites to the tumor beyond a critical size. Tumor angiogenesis is a highly regulated process that is controlled physiologically by the tumor microenvironment and genetically by alteration of several oncogenes or tumor suppressor genes. We will focus on recent demonstrations regarding the involvement of the retinoblastoma family proteins (phosphorylated retinoblastoma (pRb), p107 and pRb2/p130) at different levels of the angiogenic process. pRb and its homologs can regulate the expression of pro-and antiangiogenic factors, such as the vascular endothelial growth factor, through an E2F-dependent mechanism. Moreover, pRb is able to modulate also the transcriptional activity of several angiogenesis-related factors like HIF-1, Id2 and Oct-1. pRb2/p130 is required for both differentiation and mobilization of bone marrow-derived endothelial cell precursors and endothelial sprouting from neighboring vessels. The involvement of the pRb pathway in the angiogenesis process has also been demonstrated by different cellular models expressing viral oncoproteins, like human papilloma virus. Moreover, some natural and synthetic compounds demonstrate their antiangiogenetic activity with a mechanism of action involving pRb. Finally, the possible prognostic value of immunohistochemical evaluation of pRb and/or pRb2/p130 expression can represent a useful tool for the characterization of the angiogenic phenotype of specific tumor histotypes.

show abstract

Regulation of FGF receptor-2 expression by transcription factor E2F-1

Cited by 37 publications

References 20 publications

Coordination of cell growth and cell division: a mathematical modeling study

Coordination of cell growth and cell division: a mathematical modeling study

Biological reprogramming in acquired resistance to endocrine therapy of breast cancer

Involvement of RB gene family in tumor angiogenesis

Contact Info

Product

Resources

About