PELP1: A Novel Therapeutic Target for Hormonal Cancers

被引：27

作者：

Chakravarty, Dimple ^{[1
]}

Tekmal, Rajeshwar Rao ^{[1
]}

Vadlamudi, Ratna K. ^{[1
]}

机构：

[1] Univ Texas Hlth Sci Ctr San Antonio, Dept Obstet & Gynecol, San Antonio, TX 78229 USA

来源：

IUBMB LIFE | 2010年 / 62卷 / 03期

关键词：

estrogen receptor; coregulators; PELP1; hormonal signaling; therapy resistance; GLUTAMIC-ACID-RICH; RECEPTOR COACTIVATOR PELP1/MNAR; GROWTH-FACTOR REGULATION; RETRACTED ARTICLE. SEE; ESTROGEN-RECEPTOR; BREAST-CANCER; PROLINE-RICH; NONGENOMIC ACTIVITY; INTERACTING PROTEIN; COREGULATOR PELP1;

D O I：

10.1002/iub.287

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Recent studies implicate that the estrogen receptor (ER) coregulator proline-, glutamic acid-, and leucine-rich protein (PELP) 1 as playing critical roles in ER-genomic, ER-nongenomic, and ER-signaling cross talk with growth factor signaling pathways. PELP1 expression is deregulated in hormonal cancers and recent studies further elucidated the molecular mechanisms by which PELP1 regulates hormone therapy response. Although PELP1 is important for normal functions of the ER, the possibility to target ER-PELP1 axis appears to be an effective strategy for preventing hormonal carcinogenesis and therapy resistance. Thus, PELP1 may be useful as prognostic marker for hormonal cancers and PELP1 signaling may be useful to generate targeted therapeutics to overcome hormonal therapy resistance. (C) 2009 IUBMB IUBMB Life, 62(3): 163-169, 2010

引用

页码：163 / 169

页数：7

共 65 条

[21] Estrogen receptors:: How do they signal and what are their targets [J].

Heldring, Nina ;

Pike, Ashley ;

Andersson, Sandra ;

Matthews, Jason ;

Cheng, Guojun ;

Hartman, Johan ;

Tujague, Michel ;

Stroem, Anders ;

Treuter, Eckardt ;

Warner, Margaret ;

Gustafsson, Jan-Ake .

PHYSIOLOGICAL REVIEWS, 2007, 87 (03) :905-931

[22] Polysaccharide colloidal particles as delivery systems for macromolecules [J].

Janes, KA ;

Calvo, P ;

Alonso, MJ .

ADVANCED DRUG DELIVERY REVIEWS, 2001, 47 (01) :83-97

[23] MNAR functionally interacts with both NH2- and COOH-terminal GR domains to modulate transactivation [J].

Kayahara, Midori ;

Ohanian, Jacqueline ;

Ohanian, Vasken ;

Berry, Andrew ;

Vadlamudi, Ratna ;

Ray, David W. .

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2008, 295 (05) :E1047-E1055

[24] Cloning, distribution, and colocalization of MNAR/PELP1 with glucocorticoid receptors in primate and nonprimate brain [J].

Khan, Mohammad M. ;

Hadman, Martin ;

De Sevilla, Liesl M. ;

Mahesh, Virendra B. ;

Buccafusco, Jerry ;

Hill, William D. ;

Brann, Darrell W. .

NEUROENDOCRINOLOGY, 2006, 84 (05) :317-329

[25] Extranuclear Coactivator Signaling Confers Insensitivity to Tamoxifen [J].

Kumar, Rakesh ;

Zhang, Hao ;

Holm, Caroline ;

Vadlamudi, Ratna K. ;

Landberg, Goran ;

Rayala, Suresh K. .

CLINICAL CANCER RESEARCH, 2009, 15 (12) :4123-4130

[26] Mechanisms involved in the regulation of histone lysine demethylases [J].

Lan, Fei ;

Nottke, Amanda Clair ;

Shi, Yang .

CURRENT OPINION IN CELL BIOLOGY, 2008, 20 (03) :316-325

[27] Combination therapy with aromatase inhibitors: the next era of breast cancer treatment? [J].

Leary, A. ;

Dowsett, M. .

BRITISH JOURNAL OF CANCER, 2006, 95 (06) :661-666

[28]

Lewis-Wambi Joan S, 2005, Breast Dis, V24, P93

[29] Nongenomic actions of steroid hormones [J].

Lösel, R ;

Wehling, M .

NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2003, 4 (01) :46-56

[30] Steering estrogen signals from the plasma membrane to the nucleus: Two sides of the coin [J].

Manavathi, B ;

Kumar, R .

JOURNAL OF CELLULAR PHYSIOLOGY, 2006, 207 (03) :594-604

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