AP-1 blockade in breast cancer cells causes cell cycle arrest by suppressing G1 cyclin expression and reducing cyclin-dependent kinase activity. (Q40481763)

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English	AP-1 blockade in breast cancer cells causes cell cycle arrest by suppressing G1 cyclin expression and reducing cyclin-dependent kinase activity.	scientific article

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1 January 2020

AP-1 blockade in breast cancer cells causes cell cycle arrest by suppressing G1 cyclin expression and reducing cyclin-dependent kinase activity (English)

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1 January 2020

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1 January 2020

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Yongmin Liu

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1 January 2020

Chunhua Lu

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1 January 2020

Debbie Munoz-Medellin

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1 January 2020

Heetae Kim

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1 January 2020

Powel H Brown

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1 October 2004

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1207889

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Activation of the cyclin D1 gene by the E1A-associated protein p300 through AP-1 inhibits cellular apoptosis

1 reference

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Inducible production of c-fos antisense RNA inhibits 3T3 cell proliferation

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Cyclin E and survival in patients with breast cancer

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Cyclin E overexpression, a negative prognostic factor in breast cancer with strong correlation to oestrogen receptor status

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Protective role for c-Jun in the cellular response to DNA damage

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Patterns of matrix metalloproteinase expression in cycling endometrium imply differential functions and regulation by steroid hormones

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Functional antagonism between oncoprotein c-Jun and steroid hormone receptors

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Activation and inhibition of the AP-1 complex in human breast cancer cells

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Transcriptional regulation by transforming growth factor beta of the expression of retinoic acid and retinoid X receptor genes in osteoblastic cells is mediated through AP-1.

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A c-Jun dominant negative mutant protects sympathetic neurons against programmed cell death

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Cyclin E overexpression as an independent risk factor of visceral relapse in breast cancer

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Inhibition of AP-1 transcription factor causes blockade of multiple signal transduction pathways and inhibits breast cancer growth

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AP-1 blockade inhibits the growth of normal and malignant breast cells

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Differential ligand activation of estrogen receptors ERalpha and ERbeta at AP1 sites

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Oxidative stress and AP-1 activity in tamoxifen-resistant breast tumors in vivo

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cJun overexpression in MCF-7 breast cancer cells produces a tumorigenic, invasive and hormone resistant phenotype

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The retinoic acid receptor antagonist, BMS453, inhibits normal breast cell growth by inducing active TGFbeta and causing cell cycle arrest

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Specific protection against breast cancers by cyclin D1 ablation

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Involvement of activator protein-1 (AP-1) in induction of apoptosis by vitamin E succinate in human breast cancer cells

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Identifiers

10.1038/SJ.ONC.1207889

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1 January 2020

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1 January 2020

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