The methyl-CpG-binding protein MECP2 is required for prostate cancer cell growth

scientific article published on 01 March 2006

The methyl-CpG-binding protein MECP2 is required for prostate cancer cell growth is …
instance of (P31):
scholarly articleQ13442814

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P6179Dimensions Publication ID1004035368
P356DOI10.1038/SJ.ONC.1209179
P698PubMed publication ID16331274

P50authorDavid BernardQ44039079
Tapio VisakorpiQ49957442
Jesus GilQ55472013
Didier MontéQ56872770
P2093author name stringY de Launoit
S Rizzo
P Dumont
D Hudson
F Fuks
B Quatannens
P2860cites workThe Hallmarks of CancerQ221226
Identification of c-MYC as a target of the APC pathwayQ24310637
Transcriptional repression by the methyl-CpG-binding protein MeCP2 involves a histone deacetylase complexQ24324026
A census of human cancer genesQ24647081
MBD2 is a transcriptional repressor belonging to the MeCP1 histone deacetylase complexQ28143627
DNA methyltransferases get connected to chromatinQ28202206
Molecular determinants of resistance to antiandrogen therapyQ28236889
Myc activates telomeraseQ28505489
Methyl-CpG-binding protein, MeCP2, is a target molecule for maintenance DNA methyltransferase, Dnmt1Q28575665
The development of androgen-independent prostate cancerQ29615650
DNA hypermethylation in tumorigenesis: epigenetics joins geneticsQ33870798
A history of prostate cancer treatmentQ34013878
Molecular genetics of prostate cancer.Q34052664
Emerging connections between DNA methylation and histone acetylation.Q34298959
Polycomb complexes and silencing mechanisms.Q34320981
Histone deacetylase as a new target for cancer chemotherapy.Q34392069
DNA methyltransferase inhibitors-state of the art.Q34990742
Tumor p53 status and response to topoisomerase II inhibitorsQ35091149
The interaction of histone deacetylase inhibitors and DNA methyltransferase inhibitors in the treatment of human cancer cells.Q35137797
Strategies for reversing drug resistanceQ35567287
The molecular genetics of prostate cancer.Q35579585
Androgen receptor: a key molecule in the progression of prostate cancer to hormone independenceQ35645358
DNA methylation in prostate cancerQ35885689
Transcriptional regulation of prostate kallikrein-like genes by androgenQ38329109
Myc confers androgen-independent prostate cancer cell growthQ40271517
Preferential response of cancer cells to zebularine.Q40523300
The methyl-CpG-binding protein MeCP2 links DNA methylation to histone methylationQ40690782
Lack of RB protein correlates with increased sensitivity to UV-radiation-induced apoptosis in human breast cancer cellsQ40850195
p53 oncogene mutations in three human prostate cancer cell linesQ41586000
DNA damaging agents induce expression of Fas ligand and subsequent apoptosis in T lymphocytes via the activation of NF-kappa B and AP-1.Q46784718
Androgen receptor represses the neuroendocrine transdifferentiation process in prostate cancer cellsQ47875189
Functional analyses of MeCP2 mutations associated with Rett syndrome using transient expression systemsQ48693103
Dysregulated expression of beta-catenin marks early neoplastic change in Apc mutant mice, but not all lesions arising in Msh2 deficient mice.Q53415845
Deficiency of Mbd2 suppresses intestinal tumorigenesisQ57247922
Androgen-Independent Prostate Cancer Is a Heterogeneous Group of DiseasesQ57693579
Prostatic carcinoma: histological and immunohistological factors affecting prognosisQ68578366
The course of neuroendocrine differentiation in prostatic carcinomas. An immunohistochemical study testing chromogranin A as an "endocrine marker"Q69794650
Small cell carcinoma of the prostate. Part I. A clinicopathologic study of 20 casesQ70169490
Regressive changes and neuroendocrine differentiation in prostate cancer after neoadjuvant hormonal treatmentQ73459527
Prostate cancerQ73703143
DNA methylation and cancerQ74559063
Neuroendocrine differentiated small cell carcinoma presenting as recurrent prostate cancer after androgen deprivation therapyQ77651935
Differential posttranscriptional regulation of androgen receptor gene expression by androgen in prostate and breast cancer cellsQ77932887
Neuroendocrine differentiation in hormone refractory prostate cancer following androgen deprivation therapyQ79920255
Molecular mechanisms of prostate cancerQ80101555
P433issue9
P921main subjectcell growthQ189159
prostate cancerQ181257
P304page(s)1358-1366
P577publication date2006-03-01
P1433published inOncogeneQ1568657
P1476titleThe methyl-CpG-binding protein MECP2 is required for prostate cancer cell growth
P478volume25

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cites work (P2860)
Q36394208A Tox21 Approach to Altered Epigenetic Landscapes: Assessing Epigenetic Toxicity Pathways Leading to Altered Gene Expression and Oncogenic Transformation In Vitro
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Q93065274DNA Methylation Readers and Cancer: Mechanistic and Therapeutic Applications
Q34998222DNA binding restricts the intrinsic conformational flexibility of methyl CpG binding protein 2 (MeCP2).
Q31097619Functional Profiling of Human MeCP2 by Automated Data Comparison Analysis and Computerized Expression Pathway Modeling
Q37334003Functional connection between deimination and deacetylation of histones
Q39709698Insights into the role of DNA methylation in disease through the use of mouse models
Q34333224Knock-down of methyl CpG-binding protein 2 (MeCP2) causes alterations in cell proliferation and nuclear lamins expression in mammalian cells
Q38646785MECP2 expression in gastric cancer and its correlation with clinical pathological parameters
Q37376407MECP2 promotes the growth of gastric cancer cells by suppressing miR-338-mediated antiproliferative effect
Q36803783Mechanisms of disease: methyl-binding domain proteins as potential therapeutic targets in cancer
Q24324098Methyl-CpG-binding protein 2 is phosphorylated by homeodomain-interacting protein kinase 2 and contributes to apoptosis
Q37783909MicroRNA dysregulation in gastric cancer: a new player enters the game
Q35040740MicroRNA-4723 inhibits prostate cancer growth through inactivation of the Abelson family of nonreceptor protein tyrosine kinases
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Q55082285Peptide SA12 inhibits proliferation of breast cancer cell lines MCF-7 and MDA-MB-231 through G0/G1 phase cell cycle arrest.
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