Estrogens and progesterone promote persistent CCND1 gene activation during G1 by inducing transcriptional derepression via c-Jun/c-Fos/estrogen receptor (progesterone receptor) complex assembly to a distal regulatory element and recruitment of cyclin D1 to its own gene promoter

被引:136
作者
Cicatiello, L
Addeo, R
Sasso, A
Altucci, L
Petrizzi, VB
Borgo, R
Cancemi, M
Caporali, S
Caristi, S
Scafoglio, C
Teti, D
Bresciani, F
Perillo, B
Weisz, A
机构
[1] Univ Naples 2, Dipartimento Patol Gen, I-80138 Naples, Italy
[2] Univ Messina, Dipartimento Patol & Microbiol Sperimentale, I-98125 Messina, Italy
[3] CNR, Ist Sci Alimentaz, I-83100 Avellino, Italy
关键词
D O I
10.1128/MCB.24.16.7260-7274.2004
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
Transcriptional activation of the cyclin D1 gene (CCND1) plays a pivotal role in G(1)-phase progression, which is thereby controlled by multiple regulatory factors, including nuclear receptors (NRs). Appropriate CCND1 gene activity is essential for normal development and physiology of the mammary gland, where it is regulated by ovarian steroids through a mechanism(s) that is not fully elucidated. We report here that CCND1 promoter activation by estrogens in human breast cancer cells is mediated by recruitment of a c-Jun/c-Fos/estrogen receptor alpha complex to the tetradecanoyl phorbol acetate-responsive element of the gene, together with Oct-1 to a site immediately adjacent. This process coincides with the release from the same DNA region of a transcriptional repressor complex including Yin-Yang 1 (YY1) and histone deacetylase I and is sufficient to induce the assembly of the basal transcription machinery on the promoter and to lead to initial cyclin D1 accumulation in the cell. Later on in estrogen stimulation, the cyclin D1/Cdk4 holoenzyme associates with the CCND1 promoter, where E2F and pRb can also be found, contributing to the long-lasting gene enhancement required to drive G(1)-phase completion. Interestingly, progesterone triggers similar regulatory events through its own NRs, suggesting that the gene regulation cascade described here represents a crossroad for the transcriptional control of G(1)-phase progression by different classes of NRs.
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页码:7260 / 7274
页数:15
相关论文
共 69 条
[51]   Rb interacts with TAF(II)250/TFIID through multiple domains [J].
Shao, ZH ;
Siegert, JL ;
Ruppert, S ;
Robbins, PD .
ONCOGENE, 1997, 15 (04) :385-392
[52]   Cancer cell cycles [J].
Sherr, CJ .
SCIENCE, 1996, 274 (5293) :1672-1677
[53]   CYCLIN D1 PROVIDES A LINK BETWEEN DEVELOPMENT AND ONCOGENESIS IN THE RETINA AND BREAST [J].
SICINSKI, P ;
DONAHER, JL ;
PARKER, SB ;
LI, TS ;
GARDNER, H ;
HASLAM, SZ ;
BRONSON, RT ;
ELLEDGE, SJ ;
WEINBERG, RA .
CELL, 1995, 82 (04) :621-630
[54]   Two-dimensional gel electrophoresis analyses identify nucleophosmin as an estrogen regulated protein associated with acquired estrogen-independence in human breast cancer cells [J].
Skaar, TC ;
Prasad, SC ;
Sharareh, S ;
Lippman, ME ;
Brünner, N ;
Clarke, R .
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY, 1998, 67 (5-6) :391-402
[55]   THE UBIQUITOUS OCTAMER-BINDING PROTEIN OCT-1 CONTAINS A POU DOMAIN WITH A HOMEO BOX SUBDOMAIN [J].
STURM, RA ;
DAS, G ;
HERR, W .
GENES & DEVELOPMENT, 1988, 2 (12A) :1582-1599
[56]   Characterization of the physical interaction between estrogen receptor α and JUN proteins [J].
Teyssier, C ;
Belguise, K ;
Galtier, F ;
Chalbos, D .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (39) :36361-36369
[57]   Unlocking the mechanisms of transcription factor YY1: are chromatin modifying enzymes the key? [J].
Thomas, MJ ;
Seto, E .
GENE, 1999, 236 (02) :197-208
[58]   MAMMARY HYPERPLASIA AND CARCINOMA IN MMTV-CYCLIN D1 TRANSGENIC MICE [J].
WANG, TC ;
CARDIFF, RD ;
ZUKERBERG, L ;
LEES, E ;
ARNOLD, A ;
SCHMIDT, EV .
NATURE, 1994, 369 (6482) :669-671
[59]   THE RETINOBLASTOMA PROTEIN AND CELL-CYCLE CONTROL [J].
WEINBERG, RA .
CELL, 1995, 81 (03) :323-330
[60]   OVEREXPRESSION OF CYCLIN-D MESSENGER-RNA DISTINGUISHES INVASIVE AND IN-SITU BREAST CARCINOMAS FROM NONMALIGNANT LESIONS [J].
WEINSTATSASLOW, D ;
MERINO, MJ ;
MANROW, RE ;
LAWRENCE, JA ;
BLUTH, RF ;
WITTENBEL, KD ;
SIMPSON, JF ;
PAGE, DL ;
STEEG, PS .
NATURE MEDICINE, 1995, 1 (12) :1257-1260